Week 4 (ch. 13) Flashcards
Respiratory system function
transport of o2 from air to blood and removal of co2 from the blood
carbon dioxide
a waste product from metabolism and influences acid-base balance
URT
passageway of air from atmosphere to lungs
- resident flora
LRT
where gas exchange occurs
- sterile
nasal cavity
warming and moistening of air, foriegn material trapped by mucous secretions
nasopharynx
pharyngeal tonsils in posterior wall
palatine tonsils
lymphoid tissue in posterior portion of the oral cavity
oropharynx
common passage for air and food
epiglottis
protects opening into larynx, closes over glottis at swallowing to prevent aspiration
larynx
2 paid of vocal cords
trachea
lined by pseudo-stratified ciliated epithelium, C-shaped rings of cartilage
Trachea branches into what
Right and left primary bronchus
- right is larger and staighter and more likely a destination for aspiration material
secondary bronchi (from inverter bronchial tree)
bronchioles
alveolar ducts
alveoli
Alveoli
lined by simple squamous epithelium and surfactant to reduce surface tension and maintain inflation
- end point for inspired air
- site of gas exchage
how many lobes to the left and right lungs have
right = 3 left = 2
what is each lung covered with?
pleural membrane
thorax
provides a rigid protection wall for the lungs
- external and internal intercostal muscles move thoracic structures during ventilation
ventilation depends on what
Pressure gradient (Boyle law) - air always moves from high pressure to low pressure
– atmospheric pressure higher than pressure in alveoli (inspiration)
– pressure in alveoli is higher than in atmosphere (expiration)
pulmonary volumes is what
measure of ventilatory capacity
tidal volume
amount of air exchanged with quiet inspiration and expiration
residual volume
volume of air remaining in lungs after maximum respiration
vital capacity
max. amount of air that can be moved in and out of lungs with a single forced inspiration and expiration
where are the primary control centers for breathing location
medulla and pons
what detect changes in carbon dioxide level, hydrogen ion, and o2 levels in blood or CSF
chemoreceptors
central vs peripheral chemoreceptors
central - located in medulla
peripheral - located in carotid bodies
hypercapnia
co2 levels in blood increase
co2 can easily diffuse into CSF
– lowers pH and stimulates respiratory center
– increased rate of respirations (hyperventilation)
–causes respiratory acidosis
hypoxemia
decrease in o2
- chemoreceptors respond
- important control mechanism in individuals with chronic lung disease - move to hypoxic drive
hypocapnia
Caused by low co2 concentration (low partial pressure of co2)
- may be caused by hyperventilation (excessive amounts of co2 expired)
- causes respiratory alkalosis
external respiration
flow of gases between the alveolar air and blood
gas exchage depends on what
relative concentrations (partial pressure) of the gases
Po2 =
Pco2 =
partial pressure of o2
partial pressure of co2
Dalton law
each gas in a mixture moves along its partial pressure gradient, independent of other gases
pulmonary arteries
bring venous blood from right ventricles to be oxygenation
pulmonary capillaries
where diffusion or gas exhange occurs
pulmonary veins
return oxygenated blood to let atrium of heart
where do the left ventricle and left atrium lead to
into aorta out to systemic circulation
what factors influence the diffusion of gases?
- Partial pressure gradient
- Thickness of respiratory membrane
- - fluid accumulation in alveoli or interstitial tissue - Total surface area available for diffusion
- - if part of alveolar wall is destroyed, surface area is reduced –> less gas exchange - ventilation-perfusion ratio
- - ventilation (air flow) and perfusion (blood flow) need to match for maximum gas exhange
Describe the transport of o2
About 1% is dissolved in plasma
– most is reversibly bound to hemoglobin by iron molecules
binding and release of o2 to hemoglobin is dependent on what?
Po2, Pco2, temp, plasma pH
describe the transport of co2
about 7% dissolved in plasma
about 20% reversibly bound to hemoglobin
most diffused into RBC - converted into bicarbonate ions
how does co2 play role in control of blood ph
through bicarbonate buffer system
Diagnostic test: Spirometry
Pulmonary function test (PFT)
- test pulmonary volumes and airflow times
Diagnostic test: arterial blood gas determination
checks o2, co2, bicarbonate, serum pH
Diagnostic test: Oximetry
measures o2 saturation
Diagnostic test: exercise tolerance testing
for patients with chronic pulmonary disease
Diagnostic test: radiography
helpful in evaluating tumors and evaluate infections
What are some other diagnostic tests for respiratory function
Bronchoscopy Biopsy check site of lesion or bleeding culture and sensitivity tests sputum testing and presence of pathogens Determine antimicrobial sensitivity of pathogen
Sneezing
Reflex response to irritation in URT
– assists in removing irritants, associated with inflammation or foreign material
coughing
irritation caused by nasal drainage, inflammation or foreign material LRT caused by inhaled irritants
Sputum: thin, clear colorless
normal
Sputum: yellowish, green, thick, cloudy
bacterial
Sputum: rusty or dark
pneumococcal pneumonia
Sputum: purulent (pus like), foul odor
bronchiectasis
Sputum: Thick, tenacious (sticky) mucus
asthma or cystic fibrosis patients
Sputum: hemoptysis; bright red blood tinged frothy sputum
= pulmonary edema
Breathing patterns and sounds: Eupnea
normal rate
Breathing patterns and sounds: Kussmaul Respirations
Deep rapid respirations - typical for acidosis; may follow strenuous exercise
Breathing patterns and sounds: labored respiration or prolonged inspiration or expiration
often associated with obstruction of airways
Breathing patterns and sounds: wheezing or whistling sounds
indicate obstruction in small airways
Breathing patterns and sounds: Stridor
high pitched crowing noise (usually indicate upper airway obstruction)
Breathing patterns and sounds: Rales
light, bubbly, or crackling sounds with serous secretion
Breathing patterns and sounds: Rhonchi
Deeper or harsher sounds from thicker mucus
Breathing patterns and sounds: Absence
non aeration or lung collapse
Dyspnea
feel like you cannot inhale enough air
- subjective feeling
- may be caused by co2 or hypoxemia, often noted on exertion, such as climbing stairs
How is severe dyspnea indicative of respiratory distress?
flaring of nostrils, use of accessory respiration muscles, retraction of muscles between or above ribs
orthopnea
trouble breathing when lying down
- usually caused by pulmonary congestion
Paroxysmal nocturnal dyspnea
sudden acute type of dyspnea
- common in patients with left-sided congestive heart failure
Cyanosis
bluish coloring of skin and mucous membranes
- caused by large amounts of unoxygenated hemoglobin in blood
Pleural pain
results from inflammation or infection of parietal pleura
friction rub
soft sound produced as rought, inflamed or scarred pleural move against each other
Clubbed digits
painless, firm, fibrotic enlargement at the end of the digit
- results from chronic hypoxia associated with respiratory or CV diseases
Hypoxemia vs hypercapnea
Hypoxemia - inadequate o2 in blood
hypercapnea - increased co2 in blood
infectious diseases of the URT
common cold sinusitis epiglottitis influenze scarlet fever
URT: Common cold
Viral infection; spread through respiratory droplets
common cold symptoms
congestion, sore throat, headache, fever, malaise, cough, may see pharyngitits, laryngitis, or acute bronchitis
– symptomatic treatment
what secondary bacterial infections may occur from a common cold
Usually caused by streptococci
Purulent exudate; systemic signs (fever)
Can lead to rheumatic fever or group A beta hemolytic Streptococcus pneumoniae
URT: Sinusitis
usually bacterial infectors
analgesics for headache and pain
course of antibiotics often required
URT: Laryngotracheobronchitis (croup)
common viral infection, particularily in children
- common causative organism
- parainfluenza viruses and adenoviruses
infection usually self limited
URT: Epiglottitis
Caused by Haemophilus influenzae type B
- age 3-7, rapid onset, fever and sore throat, drooling, refuse to swallow, heightened anxiety
- swelling of larynx, supraglottic area and epiglottis - may obstruct airways
- treatment: ox2, antimicrobial therapy, intubation
URT: Influenza (FLU): what is it?
Viral infection - 3 groups of influenza virus
- type A (common), b and c
- virus constantly mutate
URT: Influenza (FLU): s/s
sudden, acute onset with fever, fatigue, aching pain in the body
– May also cause viral pneumonia, Mild case of influenza may be complicated by secondary bacterial pneumonia.
Commonly, deaths in flu epidemics result from pneumonia.
URT: Influenza (FLU): treatment
Symptomatic and supportive
- Antiviral drugs – Amantadine, Zanamivir, Oseltamivir
- Prevention highly recommended, vaccination
Scarlet Fever is caused by what
group A beta-hemolytic S. pyogenes
Scarlet fever symptoms
“strawberry tongue”
- fever, sore throat
- chills, vomiting, abdominal pain, malaise
scarlet fever treatment
antibiotics
Bronchiolitis: cause
caused by respiratory syncytial virus (RSV)
- common in children 2-12 months
Bronchiolitis: transmitted
oral droplet
Bronchiolitis: s/s
Wheezing and dyspnea, rapid shallow respirations, cough, rales, chest retractions, fever, malaise, can have severe cases`
Bronchiolitis: Treatment
Supportive and symptomatic
At risk population could have RSV immunoglobulin serum- palivizumab (synagis)
Expensive, given every 28 days through RSV season
Pneumonia: classification
Classification is based on:
- causative agent (bacteria, viral, fungal)
Anatomical location of infection
- through out both lungs, or one lobe
Pathophysiologic changes
- changes in interstitial tissue, alveolar septae, alveoli
Epidemiologic data
- nosocomial
- community acquired
Tuberculosis: causative agent
mycobacterium tuberculosis
tuberculosis: transmission
oral droplets
tuberculosis is common where
crowded living conditions, immunodeficiency, malnutrition, alcoholism, war, chronic disease, HIV/AIDS
Describe TB bacteria
acid-fast, slow growing bacillus
- somewhat resistance to drying and many disinfectants
- survive in dried sputum for weeks
- destroyed by UV lights, heat, alcohol, formaldehyde
- cell wall protects bacillus from body’s normal defenses
- normal neutrophil response does not occur
TB: Primary infection
Bacteria first enter the lungs
Local inflammatory reaction
- engulfed by macrophages (local inflammation)
if cell mediated immunity is inadequate, mycobacteria reproduce and begin to destroy lung tissue (contagious). If it is adequate, it remains small and walled off, eventually calcifying lesions called Ghon complexes (chest x-ray)
patient may stay viable in dormant state for years
TB: Secondary or reinfection
Stage of active infection
- can be years after primary infection
- occurs when host resistance is decreased
- organisms multiple - tissue destruction - large area of necrosis; cavitation occurs
- spread to other parts of lung and expelled in sputum (contagious)
TB: s/s
Anorexia, Malaise, Fatigue, Wght loss, afternoon low-grade fever & night sweats, prolonged cough becomes productive (sputum producing), sputum contains blood
TB: diagnostics
Primary TB or latent- Mantoux skin test- false positive if person received vaccination for TB (BCG)
QuantiFeron-TB Gold test – newer blood test in place of Mantoux skin test
–> Common routine in health care workers, if x-ray needed then typically every 5 years
Active TB diagnostics
Sputum culture, Acid-fast sputum test, x-ray, & CT scan, Nucleic acid amplification (NAA) test
Why is TB becoming and increasinly serious problem
homelessness (over crowding in shelters)
HIV infection
lack of health care
multidrug resisant TB
Treatment for Latent TB
Isoniazid (INH)
Rifapentine
Rifampin
Active TB treatment
Isoniazid Rifampin Ethambutol Pyrazinamide Streptomycin
Cystic Fibrosis
inherited disorder – gene located on chromosome 7
- -> tenacious mucus from enodocrine glands
- -> effets lung and pancrease
Cystic fibrosis: Lungs
mucus obstructs airflow and bronchioloes and small bronchi
– permanent damage to bronchial walls
Cystic fibrosis in the lungs is commonly caused by what
Pseudomonas aeruginosa and Staphylococcus aureus
cystic fribrosis: digestive trace
Meconium ileus in newborns
Blockage of pancreatic ducts
Obstruction of bile ducts
Salivary glands often mildly affected
Cystic Fibrosis: Reproductive tract
Obstruction of vas deferens (male)
Obstruction of cervix (female)
Cystic Fibrosis: sweat glands
sweat has high sodium chloride content
Cystic Fibrosis: s/s
a. Meconium ileus may occur at birth.
b. Salty skin
c. Signs of malabsorption
d. Chronic cough and frequent respiratory infections
e. Failure to meet normal growth milestones
Cystic Fibrosis: Diagnosis
genetic testing sweat test testing of stool radiography, pulmonary function blood gas analysis
Cystic Fibrosis treatment
Replacement therapy and well-balanced diet
Chest physiotherapy – postural drainage, percussion, coughing techniques - Daily
Aspiration s/s
coughing and choking loss of voice stridor and horsness wheezing tachcardia and tachpnea nasal flaring, chest retrations, hypoxia cardiac or respiratory arrest
aspiration treatment
swallow study
keep objects away from children
Asthma
Bronchial obstruction
- occurs in persons with hypersensitive and hyperresponsive airways
Asthma pathophysiology
changes in bronchi and bronchioles
- inflammation of the mucosa with edema
- bronchoconstriction caused by contraction of smooth muscle
increased secretion of thick mucus in airways
extrinsic asthma
acute episodes triggered by type 1 hypersensitivity reactions
intrinsic asthma
onset during adulthood
hyperresponsive tissue in airway initiates attact
asthma stimuli
Respiratory infections, Stress, Exposure to cold, Inhalation of irritants, Exercise, Drugs
asthma s/s
cough dyspnea tight feeling chest wheezing rapid and labored breathing expulsion of thick / sticky mucus tachycardia hypoxia
respiratory alkalosis caused by
hyperventilation
respiratory acidosis cause
air trapping
severe respiratory distress leads to
hypoventilation leads to hyperoxemia and respiratory acidosis
respitatory failure indicated by what
decreasing responsiveness, cyanosis
chronic asthma attacks can lead to
chronic asthma and COPD
- bronchial wall thickening and fibrous tissue
Asthma: Acute episode
Persistent severe attack of asthma
- does not respond to usual therapy
- medical emergency
- may be fatal because of severe hypoxia and acidosis
Asthma treatment: general measures
Skin tests for allergic reactions Avoidance of triggering factors Good ventilation of environment Swimming and walking Use of maintenance inhalers or drugs
Asthma treatment: measure for acute attacks
controlled breathing tech.
inhalers
glucocorticoids
Asthma treatment: measures for status Asthma asthmaticus
hospital care if no response to bronchodilator
Asthma treatment: prophylaxis and treatment for chronic asthma
Leukotriene receptor antagonist
- block inflammation response in presence of stimulus
- not effective for treatment f acute attacks
Asthma treatment: Cromolyn sodium
Prophylactic medication
Inhalation on a daily basis
Useful for athletes and sports enthusiasts
No value during an acute attack
COPD may lead to the development of what
corpulmonale (right sided heart failure)
What is COPD Emphysema
Destruction of alveolar walls and septae
–> leads to large, permanent inflated alveolar air spaces
COPD Emphysema is classified by what
specific location of changes
COPD Emphysema contributing factors
genetic, gender, smoking, bacteria
COPD Emphysema: breakdown of alveolar wall results in what
loss of surface area for gas exchange.- loss of pulmonary capillaries.- loss of elastic fibers.- altered ventilation-perfusion ratio.- decreased support for other structures.
COPD emphysema: fibrosis
Narrowed airways, Weakened walls, Interference with passive expiratory airflow
COPD Emphysema: describe the progressive difficulty with expiration
a. Air trapping and increased residual volume
b. Overinflation of the lungs
c. Fixation of ribs in an respiratory position, increased anterior-posterior diameter of thorax (barrel chest)
d. Flattened diaphragm (on radiograph
COPD Emphysema: describe how advanced emphysema leads to loss of tissue
Adjacent damaged alveoli coalesce, forming large air spaces.
Pneumothorax
–> Occurs when pleural membrane surrounding large blebs ruptures
Hypercapnia becomes marked.
Hypoxia becomes driving force of respiration.
Frequent infections
Pulmonary hypertension and cor pulmonale
may develop in late stage
Emphysema s/s
Dyspnea (first on exertion and worsens with disease progression)
hyperventilation w prolonged expiratory phase (barrel chest)
Anorexia / fatigue
Clubbed fingers
Emphysema diagnosis
Chest radiography
pulmonary function tests (PFT)
Emphysema treatment
- Avoid respiratory irritants
- Immunization
- Pulmonary rehabilitation
- Breathing techniques
- nutrition and hydration
- Bronchodilators, antibiotics, oxygen therapy as condition advances
- Lung reduction surgery
COPD chronic bronchitis
inflammation, obstruction, repeated infection, chronic coughing twice for 3 months or longer in 2 years
Patho of chronic bronchitis
Mucosa inflammed and swollen
hypertrophy and hyperplasia of mucous glands
fibrosis and thickening of bronchial walls
chronic bronchitis s/s
a. Constant productive cough
b. Tachypnea and shortness of breath
c. Frequent thick and purulent secretions
d. Cough and rhonchi more severe in the morning
e. Hypoxia, cyanosis, hypercapnia
f. Polycythemia, weight loss, signs of cor pulmonale possible
g. As vascular damage and pulmonary hypertension progress
Chronic bronchitis treatment
Stop smoking / irritant exposure treat infection vaccination expectorants bronchodilator chest therapy low-flow o2 nutritional supplements
Vascular disorders: pulmonary edema what is it
fluid collecting in alveoli and interstitial area
- results from primary conditions
- reduced amount of o2 diffusing into blood
- interferes with lung expansion
Vascular disorders: pulmonary edema may develop when
a. Inflammation in lungs is present.
- Increases permeability of capillaries
b. Plasma protein levels are low.
- Decreases osmotic pressure of plasma
c. Pulmonary hypertension develops.
Vascular disorders: pulmonary edema s/s for mild and chronic
Mild: cough, orthopnea, rales
chronic:
- hemoptysis often occurs
- frothy sputum
- labored breathing
- hypoxemia increased
- cyanosis
Vascular disorders: pulmonary edema treatment
treat causative factors
supprtive care
possibly positive pressure mechanical care
keep upper body elevated
Pulmonary embolus treatment
Stockings surgery heparin or stretokinase mechanical ventilation embolectomy
pulmonary embolism diagnosis
Radiography
Lung scan
MRI
Pulmonary angiography
Pleural Effusion: what
Prescence of excessive fluid in pleural cavity
– causes increase pressure in pleural cavity and separation of pleural membrances
Pleural effusion: Exudate effusion
response to inflammation
Pleural effusion: transudate effusions
Watery effusions (hydrothorax) - result of increased hydrostatic pressure or decreased osmotic pressure in blood vessles
Pleural effusion: s/s
Dyspnea
chest pain
increase RR and HR
usually dullness to percussion and absense of breath sounds over the affected area
tracheal deviation
hypotension
Pleural effusion: treatment
Remove underlying cause to treat respiratory impairment.
Analyze fluid to confirm cause
Chest drainage, thoracocentesis to remove fluid and relieve pressure
pneumothorax is what
air in pleural cavity
Describe a closed pneumothorax
air can enter pleural cavity from internal airways - no opening in chest well
closed pneumothorax: simple of spontaneous pneumothorax
tear on the surface of the lung
closed pneumothorax: secondary pneumothorax
associated with underlying respiratory disease
Rupture of an emphysematous bleb on lung surface or erosion by a tumor or tubercular cavitation
Open pneumothorax: what is it
Atmospheric air enters the pleural cavity through an opening in the chest wall
“sucking” wound – large opening in chest wall
Open pneumothorax: tension pneumothorax
results of an opening through chest wall and parietal pleura or from a tear in the lung tissue and visceral pleura
- air enters pleural cavity on inspiration but hole closes on expiration
- trapping air leads to increase pleural pressure and atelectasis
- most serious
Pneumothorax s/s
Atelectasis dyspnea cough chest pain reduced breath sounds unequal check expansion hypoxia interference with venous returne
pneumothorax treatment
Hospital ASAP
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Infant respiratory syndrome usually results from what
premature birth
Infant respiratory syndrome what is it
lack of surfactant in alveoli
Infant respiratory syndrome pathophysiology for Poorly developed alveoli that are diff. to inflate
- diffuse atelectasis results
- - decrease pulm. blood flow, pulmonary vasoconstriction –> hypoxia
Infant respiratory syndrome pathophysiology for poor lung perfusion and lack of surfactant
Increased alveolar capillary permeability
– fluid and protein are leaking into the interstitial area and alveoli, hyaline membrane formation
Infant respiratory distress syndrom s/s
Respiratory difficulties at birth
Resp. = rapid and shallow
Frothy sputum
expiratory grunt
BP falls
cyanosis
peripheral edema
servere hypoxemia and decreased responsiveness
irregular respirations with periods of apnea
Infant respiratory distress syndrom diagnostic tests
arterial blood gas analysis
Infant respiratory distress syndrome treatment
Glucocorticoids for women in premature labor
Synthetic surfactant for high-risk neonate
CPAP
o2 therapy
Adult respiratory distress syndrome
results from injury to the alveolar wall and capillary membrane
what does Adult respiratory distress syndrome lead to
Release of chemical mediators
– increased permability of alveolar capillary membranes
- increase fluid and protein in interstitial area and alveoli
- damage to surfactant producing cells
- diffuse necrosis and fibrosis if patient survives
Adult respiratory distress syndrome s/s
dyspnea restlessness rapid, shallow respirations increase HR combination of metabolic and resp. acidosis
Adult respiratory distress syndrome treatment
treat underlying cause
supportive respiratory therapy
