respiratory Flashcards
upper respiratory tract
outside thorax Oronasopharynx Pharynx Larynx Upper trachea
lower respiratory tract
within thorax Lower trachea Bronchi Bronchioles Alveolar duct Alveoli
conducting zone
nose to bronchioles
respiratory zone
alveolar duct to alveoli
trachea
consists of 20 rings of cartilage, each backed with muscle and connective tissue, and lined with smooth tissue; lengthens and widens with each breath in and returning to normal with breath out
epiglottis
prevents food from entering the tracheobronchial tree by closing over the glottis during swallowing
bronchi
airways of smooth muscle leading from trachea into lungs and branching into bronchioles
bronchioles
contain smooth muscle and no cartilage; and depend on the elastic recoil of the lung for patency. Each is capped with an alveolus cluster.
alveoli
are the basic units of gas exchange; tiny, balloon-shaped air sacs in clusters at the end of the respiratory tree
Type I alveolar cells (pneumocytes) – responsible for the exchange of oxygen and carbon dioxide
Type II alveolar cells (pneumocytes) – are in the walls of the alveoli and secrete surfactant, a phospholipid protein that reduces the surface tension in the alveoli; without surfactant, the alveoli would collapse
Alveolar macrophages – phagocytize/eliminate foreign particles, dead cells, bacteria
accessory muscles of respiration
include Scalene, Pectoralis, Trapezius, Sternocleidomastoid, and Rectus abdominis muscles
inhalation and expiration
Breathing in brings oxygen into lungs. The lungs remove the oxygen and pass it through to the bloodstream, where it is carried to the heart, and to tissues and organs.Breathing out removes the carbon dioxide in the lungs, from the blood from the body.
diaphragm is the main
respiratory muscle
intercostal muscles expand and contract the thoracic space to
facilitate breathing
when you breathe in the diaphragm
pulls downward (contracts), creating a vacuum that causes a rush of air into your lungs; external intercostal muscles contract
when you breathe out the diaphragm
relaxes upward, pushing on your lungs, allowing them to deflate; internal intercostal contract and external intercostal muscles relax. Expiration occurs from passive, elastic recoil of lungs, rib cage and diaphragm
forced/active inspiration
Sternocleidomastoid muscle elevates sternum
Scalene muscles elevate ribs
Pectoralis minor elevates ribs
Trapezius retract scapula to expand thoracic cavity
Diaphragm contracts more
forced/active expiration
Rectus abdominis contract to push diaphragm up
Internal intercostals contract to compress lungs
ventilation perfusion mismatch
Decreased when there is decreased ventilation in lungs or increased perfusion (ie. More blood flow to lungs)
Increased when there is increased ventilation or decreased perfusion (ie. Less blood flow to lungs)
v/q ratio
The amount of air that reaches the alveoli divided by the amount of blood flow in the capillaries of the lungs
Normal V/Q ratio = 0.8
4 liters of oxygen pass through lungs each minute – ventilation
5 liters of blood pass through capillaries of lungs every minute – perfusion
ratio of amount of air reaching the alveoli per minute to the amount of blood reaching alveoli per minute
v/q mismatch occurs when
ratio is higher or lower
- hypoxemia: below normal levels of oxygen in arterial blood and can lead to tissue hypoxia - V/Q mismatch in ventilation and perfusion can arise due to either reduced ventilation of part of the lung or reduced perfusion
reduced ventilation
Pneumonia – alveoli filled with exudate and unable to maintain ventilation
Asthma
COPD
V/Q ratio <1
reduced perfusion of lungs
Pulmonary embolism – areas of pulmonary circulation obstructed, limiting blood flow to alveoli
Emphysema
V/Q ratio >1
TLC
Total lung capacity – the volume in the lungs at maximal inflation
FEV
Forced expiratory volume test – measures how much air a person can exhale in a forced breath
FVC
Forced vital capacity – total amount of air exhaled during the FEV test
FRC
Functional Reserve Capacity – the volume of air in the lungs when the respiratory muscles are fully relaxed and no airflow is present; determined by the balance of the inward elastic recoil of the lungs and the outward elastic recoil of the chest wall
tidal volume
the normal volume of air displaced between normal inhalation and exhalation; 500ml per inspiration for young adult [7ml/kg of body mass]
diffusing capacity
a measure of how well oxygen and carbon dioxide transfer/diffuse between the lungs and blood
adventitious breath sounds
crackles
wheezes
rhonchi
crackles
Air flowing by liquid
Fine are high-pitched crackling/Velcro
Coarse are low-pitched and gurgling
Sound drier higher in bronchial tree and wet lower in the bronchial tree
wheezes
Air flowing though constricted airways or an obstruction
High-pitched musical sound
Continuous
rhonchi
Air flowing over thick secretions
Low-pitched sound
Continuous
Deep and low-pitched over the larger bronchi
alveolus
a sac that fills with air when we breathe in and allows air to pass across a membrane into a blood vessel (the alveolar capillary). Then, the sac contracts and deflates letting carbon dioxide out.
airway
trachea, bronchi, bronchioles
alveolar membranes
Allow oxygen to cross to the blood and carbon dioxide to cross out from the blood.
pulmonary blood vessels
bring blood to the lungs to pick up oxygen and release carbon dioxide
alveolar sac filled with something other than air
Pus as in pneumonia OR fluid with edema or blood
Prevents alveoli to hold normal oxygen and thus, decreases ability to adequately oxygenate blood in their capillaries
alveolar sac does not open adequately
Prevents adequate inspiration decreases amount of oxygen taken in
alveolar sac unable to expire due to obstruction or decreased elastic recoil of sac
Prevent alveoli from fully deflating and can lead to retention of carbon dioxide; and blocking initiation of new breathing cycle
destruction or thickening of membrane reduces
the diffusion of oxygen across it
Decreased surface area available for gas exchange
loss of portions of membrane can occur with
emphysema
thickening of membrane results from
fibrosis of the lungs
Connective tissue disease
Hypersensitivity
Exposure diseases—silicosis, asbestosis
obstruction of blood vessels by pulmonary embolus prevents
transport of blood to the lungs for gas exchange
pulmonary hypertension results from
rise in blood pressure in the pulmonary arteries due to changes in the cells that line the vessels Artery walls can become stiff and thick Extra tissue may form Vessels can become inflamed Blood flow becomes restricted or blocked
types of lung disease
-Obstructive: create difficulty for air to get out-Restrictive: cause difficulty for air to get in
examples of obstructive lung disease
Mechanical obstruction of airway: foreign object, tumour, chronic mucus plug as in bronchitis
Increase resistance in the airways: airway thickening from inflammation in chronic bronchitis
Increased tendency for airway closure: asthma, emphysema
examples of restrictive lung disease
Stiff lungs: interstitial lung disease
Stiff chest wall: kyphoscoliosis, obesity
Respiratory muscle weakness: neuromuscular disease
obstructive lung disease
Lungs feel full
Wheezing
Mucus production
If airways obstructed, alveoli cannot contract well, making it hard to get the air out:
Total Lung Capacity and Residual Volume and Functional Residual Capacity increased
restrictive lung disease
Feels hard to breathe enough air
Breathing difficulties may cause panic
If airways/chest restricted/limited, alveoli cannot expand well, making it hard to get air in:
Total Lung Capacity and Residual Volume and Functional Residual Capacity decreased
disorders of the lower respiratory system
bronchopulmonary dysplasia (BPD) cystic fibrosis (CF)
BPD occurs in
premature/low birth weight infants having persistent respiratory problems, requiring respiratory support
Underdevelopment of lungs in premature infant leading to need for oxygen and/or mechanical ventilation
Result of damage to lungs caused by mechanical ventilation and long-term oxygen use
Air pressure from ventilation damages fragile airways
Large amounts of oxygen damage the lining of the bronchi and alveoli
Infections
Chest wall or muscle weakness
Aspiration
risk factors for BPD
Preterm delivery < 28 weeks
Birth weight < 1500 grams
Maternal womb infection (choriamnionitis)
Postnatal sepsis or pneumonia
Patent ductus arteriosus
Infants with small lungs (“Pulmonary hypoplasia”)
Male babies
BPD leads to
the need for supplemental oxygen and mechanical ventilation
BPD diagnosed when
When baby has trouble weaning from mechanical ventilation or requires extra oxygen at or after 36 weeks(gestational age)
Baby has cyanosis, cough, SOB
Changes on chest x-ray
babies with BPD
Have fewer alveoli
Have larger alveoli with thicker walls
Cause the baby to have to work harder to breather and get enough oxygen
clinical manifestations of BPD
Hypoxemia Increased work of breathing Hypercapnia Bronchospasm with wheezing Mucus plugging Pulmonary hypertension Tachypnea Retractions Nasal flaring Right- sided heart failure
living with BPD: chronic
Recurrent cough and wheezing are frequent
High susceptibility to repeated respiratory infections and their complications
Susceptible to viral infections and environmental exposures
Infants who survive are discharged home on home oxygen and some on ventilators
Good nutrition is required
Increased risk of asthma during childhood
Limitations on activity tolerance
Abnormal PFT’s indicate expiratory airflow obstruction and air trapping
Emotional impact of prolonged infant hospitalization for infant and parents
Compromised Pulmonary Function and defences
-can impact the circulatory system
cystic fibrosis
Characterized by abnormal thick secretions that cause obstructive problems within the respiratory, digestive, and reproductive tracts
complex multisystem illness
patho of CF
Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene
CFTR gene regulates the CFTR protein that functions as a channel across the membrane of cells that produce mucus, sweat, saliva, tears and digestive enzymes
CFTR protein regulates movement of chloride and sodium ions across epithelial cell membranes; maintains balance of salt and water
CFTR gene mutations generate CFTR protein dysfunctions – chloride becomes trapped in cells and no water hydration
Usually slippery, free-flowing mucus becomes thick and sticky
Respiratory tract and pancreas are predominantly affected.
respiratory patho of CF
Bronchioles obstructed by thick mucus secretions
Impaired cilia functioning leading to decreased mucociliary clearance
Poor clearance of bacteria inhaled leading to predisposition for lung infections
Bacterial colonization with Pseudomonas aeruginosa and Staphylococcus aureus – common in CF
Pathogens cause inflammatory response
Chronic infection and ongoing inflammatory responses lead to destruction of the airway
Increased mechanical stress from increased obstruction of airway
patho of pneumothorax with CF
Chronic infection and inflammation lead to dilation and damage to the bronchi
Airways become blocked and deformed
Cavitations or cysts, areas of brochiolar consolidation, fibrosis and air-trapping develop in the lung tissue
Air-trapping induces extra pressures in the alveolar tissue
Compromise respiratory adequacy
Blebs and bullae may develop in visceral pleura
From inflammation, irritation, and weakening of airway walls
Air leaks into pleural space exerting pressure on lung
GI tract patho in CF
Thick secretions block ducts—pancreatic insufficiency, biliary obstruction, intestinal obstruction
Pancreatic duct becomes blocked with thick mucus
Digestive enzymes accumulate in pancreas – unable to travel to the small intestine
Impaired digestion and absorption of fat (steatorrhea) and protein (azotorrhea)
Malabsorption of fat-soluble vitamins A, D, E, K
Pancreas becomes inflamed
Damage to hormone cells – glucose intolerance
Insulin dependent diabetes
Meconium ileus (MI) in newborn – obstruction of the bowel by overly thick meconium
Distal intestinal obstruction syndrome (DIOS) – intestinal obstruction
Thick/congealed intestinal contents block lumen of small intestine
Rectal prolapse
Large, bulky stools, malnutrition, poor muscle tone, colon distension and increased intra-abdominal pressure due to coughing/distended bowel
CF diagnostic evaluation
Canada-wide newborn screenings
Most cases identified through newborn screenings
Immunoreactive trypsinogen (IRT) protein levels checked
Genetic testing – mutations in CFTR
~ 10% not diagnosed until adolescence or early adulthood
Sweat chloride test – standard for confirming diagnosis
Infants >2 weeks of age [to obtain sufficient sweat]
For older children/adults [if not screened as infant]
Genetic or sweat testing with history of recurrent pancreatitis, chronic lung infections, bronchiectasis
Symptoms of chronic coughing, recurrent sinus infections, no weight gain, abnormal bowel movements, infertility
Family history – family member with CF or carrier
pulmonary manifestations in CF
Initially
Recurrent wheezing, recurrent pneumonia
Chronic/recurrent dry nonproductive cough [early], developing purulent sputum later
Over time – ongoing obstruction and mucus accumulation
Bronchiectasis
Recurrent infections, dyspnea on exertion, paroxysmal cough, hemoptysis, chest pain, recurrent sinusitis and nasal polyps
Increased anteroposterior diameter of chest (barrel-shaped); cyanosis; clubbing of fingers and toes
GI clinical manifestations in CF
Meconium ileus
Large, bulky, loose, frothy, foul-smelling stool (steatorrhea)
Rectal prolapse
Biliary cirrhosis with portal hypertension
Voracious appetite (early); loss of appetite (late)
FTT: Lack of weight gain, skeletal muscle wasting and weakness, failure to grow, distended abdomen
Thin extremities, vitamin deficiency, anemia
genitourinary manifestations with CF
Male infertility
Congenital absence of vas deferens or blocked vas deferens
Female infertility
Highly viscous cervical secretions – impede sperm travel
Malnutrition can lead to anovulation and amenorrhea
Female incontinence
Frequent coughing weakens pelvic floor muscles
using “CF PANCREAS” for presenting signs
Chronic cough and wheezing
Failure to thrive
Pancreatic insufficiency
Alkalosis and hypotonic dehydration
Neonatal intestinal obstruction (meconium ileus) Nasal polyps
Clubbing of fingers/chest radiograph with characteristics changes
Rectal prolapse
Electrolyte elevation in sweat, salty skin
Absence or congenital atresia of vas deferens
Sputum with Staph or Pseudomonas (mucoid)
idiopathic pulmonary fibrosis (IPF)
Chronic, progressive, fibrosing disorder of the lower respiratory tract (limited to lungs).
median survival for IPF
2-4 years after diagnosis
usual onset for IPF
50-70 years of age
common risk factors of IPF
Cigarette smoking Viral infection Environmental pollutants Chronic aspiration GERD: acid reflux/heartburn Genetic predisposition More common in men than women
patho of IPF
Exposure to an inciting agent (risk factors) in a susceptible host causes epithelial lung damage
Instead of initiation of normal wound healing to repair injured epithelium, abnormal activation leads to formation of fibroblastic/myofibroblastic centers – deposition and remodeling of matrix
Wound myofibroblasts which would normally apoptosize do not – leading to accumulation of myofibroblasts and excessive production of matrix proteins, fibrosis – leading to scarring and tissue stiffness/contraction
Fibrotic lung tissue reduces ability to expand leading to decreased lung compliance
Leads to increased WOB
Decreased tidal volume
Hypoventilation
Hypercapnia
Hypoxemia results from decreased diffusion of oxygen from alveoli to capillary
clinical presentation of IPF
History:
Chronic exertional dyspnea
Chronic cough, non productive
Fatigue
Physical Examination:
Bilateral “Velcro-like” crackles [fine/dry crackles]
Clubbing
Acrocyanosis [extremities]
Physiological:
Resting hypoxemia
Low diffusion capacity of the lung (DLCO)
Normal or low forced vital capacity (FVC)
Chest X-Ray
Bilateral basal abnormalities, honeycombing/reticulation [net-like] - peripheral
diagnosing IPF
History Physical examination: Dyspnea, cough, Velcro crackles Pulmonary function testing High-resolution CT Lung Biopsy [if necessary]
presentation of patient with COPD
Potential complications include: Respiratory infections Mental health High blood pressure Lung cancer Heart
emphysema
SOB = Shortness of breath
Alveoli are damaged
Over time, the inner walls of the air sacs weaken and rupture — creating larger air spaces instead of many small ones
Surface area of the lungs is reduced and the amount of oxygen that reaches the bloodstream is decreased
presentation of patient with chronic bronchitis
Most common symptom: Persistent cough [present for most days in a month lasting for 3 months with at least 2 such episodes occurring for 2 years in a row] “smoker’s cough”
Coughing up mucus (expectoration)
Wheezing
Chest discomfort
Often have a cough and make mucus for many years before they have shortness of breath
History: Possible exposure to inhaled irritants/chemicals/smoking
chronic bronchitis may lead to
Disability
Frequent and severe respiratory infections
Narrowing and plugging of
Trouble breathing
other symptoms for chronic bronchitis may include
Bluish fingernails, lips, and skin Wheezing and crackles Swollen feet Heart failure The symptoms of chronic bronchitis may look like other lung conditions or health problems
diagnostic tests for emphysema
Chest x-ray CT lung scan Alpha-1 antitrypsin (AAT) test Pulmonary function tests Include spirometry Arterial blood gas
diagnostic tests for chronic bronchitis
Chest x-ray CT lung scan Pulmonary function tests Include spirometry Arterial blood gas
pulmonary hypertensioin
Mean elevated pulmonary artery pressures (PAP) > 25 mmHg at rest or > 30 mmHg with exercise
Pulmonary arterial hypertension (PAH) if PAP caused by abnormalities in pulmonary arterioles
Pulmonary venous hypertension (PVH) if PAP caused by abnormalities that increase left atrial pressure leading to back pressure in the pulmonary circulation
pulmonary hypertension caused by
increased pulmonary vascular resistance or increased pulmonary venous pressure
pulmonary hypertension leads to
right ventricular (RV) dilation and remodeling – then RV failure and death [when RV compensation cannot sustain normal cardiac function]
patho of increased pulmonary vascular resistance
Endothelial and smooth muscle dysfunction leads to proliferation, hypertrophy and chronic inflammation AND Pathologic vasoconstriction occurs due to overproduction of vasoconstrictors and decreased production of vasodilators
Vasoconstriction leads to increase in pulmonary pressure and endothelium injuries [activating coagulation]
Lead to vascular wall remodeling resulting in fibrosis and thickening of vessel walls causing narrowing and further vasoconstriction
patho of increased pulmonary venous pressure
Result of disorders that affect left side of heart and increase pressure in the left chambers
Leads to increased pressure in the pulmonary veins
This elevated pulmonary venous pressure causes damage to the alveolar-capillary wall and leads to edema
Constant high pressure lead to thickening in the walls of the alveolar-capillary membrane and decreases diffusion
signs and symptoms of pulmonary hypertension
Often not detected until severe Early Symptoms may include: Progressive exertional dyspnea Fatigue Chest discomfort Tachypnea Later Symptoms [signs of Right heart failure] may include: Exertional presyncope Peripheral edema RV heave S3 Jugular vein distention Accentuation of the pulmonary component of the second heart sound Tricuspid regurgitation murmur
diagnosis of pulmonary hypertension
Exertional dyspnea
Initial confirmation:
Chest X-ray, spirometry, ECG to rule out other causes of dyspnea
Echocardiography (TTE) to assess RV function
CBC for erythrocytosis, anemia, thrombocytopenia
Additional tests:
V/Q, CT, pulmonary function tests
Serum autoantibody tests – to rule autoimmune
When confirmed pulmonary artery catherization to measure:
Right atrial pressure
Right ventricular pressure
Pulmonary artery pressure
Pulmonary artery occlusion pressure
Cardiac output
Left ventricular diastolic pressure
cor pulmonale
Right ventricle enlargement (hypertrophy, dilation or both)
Secondary to a lung disorder that causes pulmonary artery hypertension increasing pressure on RV and leading to RV failure
Initially asymptomatic
Symptoms of dyspnea or exertional fatigue due to underlying lung disorder
Symptoms occur with exercise when cardiac output falls
As RV pressures increase may have [Right heart failure symptoms]:
Jugular vein distention
Peripheral edema
S3 and S4
Tricuspid regurgitation murmur
Chest pain
Chest X-Ray shows enlargement of RV and pulmonary artery
ECG may show RV hypertrophy
common conditions and some general indications for lung transplants
Advanced chronic obstructive pulmonary disease [emphysema and chronic bronchitis]
Idiopathic pulmonary fibrosis
Cystic fibrosis
Idiopathic pulmonary arterial hypertension
Alpha 1-antitrypsin deficiency
Untreatable end-stage lung disease
Substantial limitation to daily activities – symptomatic with ADLs
Limited life expectancy: high risk of death to lung disease within 2 years
Ambulatory with rehabilitation potential
Acceptable nutritional status
Satisfactory psychosocial profile and emotional support system
Usually up to 65 years of age
High likelihood of surviving at least 90 days post transplant
High likelihood of 5-year post-transplant survival from general medical perspective
types of lung transplants
Lobe – usually lower lobe removed and used to replace the recipient’s diseased lung; usually two lobes different donors
Single-Lung – one lung
Double-Lung – both lungs
Heart-Lung – both lungs and heart from a single donor
Living transplant – donor must be healthy and non-smoking and good match
Cadaveric transplant – most transplants from deceased organ donors
donated lungs need to be
large enough to adequately oxygenate the recipient but small enough to fit with the chest cavity
contraindications for lung transplants
Concurrent chronic illness such as congestive heart failure, kidney disease, liver disease
Other serious health conditions that will not improve following transplant
Current or recurrent infection that cannot be treated including HIV and hepatitis
Current or recent cancer
Health conditions that impair ability to tolerate surgery
Obesity – BMI > 35 kg/m2
Chest wall or spinal deformity that causes restriction
Current use of tobacco or illegal drugs
Alcohol dependency
Psychosocial problems/Psychiatric conditions
Noncompliance with medical instructions and therapies
acute lung transplant rejection
Flu-like symptoms Fever Fatigue Dry Cough Chest pain Dyspnea on exertion Decreased oxygen saturation (with exercise) Decreased spirometry (> 10%) Chest CT: Diffuse opacities Crackles on physical examination
chronic lung transplant rejection
Causes:
Bronchiolitis Obliterans Syndrome (BOS): inflammation and scarring/thickening of airways
Restrictive allograft syndrome (RAS) – lungs decrease in size
Symptoms:
Productive cough
Dyspnea at rest
Airway Obstruction
Infections: Pseudomonas aeruginosa; Aspergillus spp
Chest CT: bronchial wall thickening; opacities
survival of lung transplant
Median survival for single-lung transplants is 4.6 years; double-lung transplants I 6.6 years Quality of life post transplant: Most recipients are able to resume an unencumbered lifestyle Over 9% report no activity limitations Causes of death include: Infection: Aspergillus and cytomegalovirus Bronchiolitis obliterans Graft failure Diffuse alveolar damage caused by: Harvest injury Acute antibody-mediated rejection Severe acute rejection Infection
