Test 3: Pulmonary Flashcards
Ventilation definition
Movement of air in and out of the lungs
Respiratory rate is actually ventilation rate
1137
Gas Exchange definition
diffusion of O2 and CO2 between alveoli in the lungs and the blood in alveolar capillaries
Driven by partial pressures of gasses (RA 20-21%)
1143-1147
Perfusion definition
movement of blood into and out of the capillary beds
1135
Transport definition
movement of O2 and CO2 via blood and circulatory system
1143-1147
What are goblet cells?
Cells of the epithelial lining of the bronchial tree that secrete mucous protecting the airway epithelium.
When they detect a microbial invasion in the bronchial tree they secrete enzymes that improve the ability of the mucus to trap them in the mucous blanket. Later is expectorated or cilia move it up.
1133
What are cillia or ciliated cells?
In the epithelial lining of the upper airways and bronchial tree that rhythmically beat the mucous blanket toward the trachea and pharynx where it can be swallowed or expectorated by coughing.
1133
Primary SYMPATHETIC neurotransmitter of the lungs, receptor type and what does it do?
Norepinephrine (& epinephrine according to the slides and organizer! Also google but Norepi is still the predominant)
Beta-adrenergic according to the book (beta 2 according to the slides & organizer… Also google who says beta 2 is a type of beta adrenergic receptor)
Bronchodilation via smooth muscle relaxation
1140
Primary PARASYMPTATHETIC neurotransmitter of the lungs, receptor type and what does it do?
Bonus info??
Acetylcholine
Muscarinic receptors M2 & M3
BronchoCONSTRICTION via smooth contraction
BONUS: Acetylcholine acts on M2 to limit the release of more acetylcholine, while it works on M3 to cause bronchoconstriction and increased mucus production (SOUNDS LIKE EXERCISE INDUCED ASTHMA HAHAHA!)
1140
**Substances produced by lung cells and endothelium that affect respiratory smooth muscle?
What do they make it do?
What oral drugs do we use to counter them?
Leukotrienes (from arachidonic acid via lipoxygenase pathway) & Histamine (mast cells)
Both cause CONSTRICTION
Leukotrienes:
-increased permeability
-asthma & allergic reactions
-singulair
Histamine:
-chemotactic & proteases
-zyrtec
lecture & organizer
What are the gas exchange airways
bronchioles
alveolar ducts
alveoli (singular alveolus)
1133
What are the pores of Kohn?
tiny passages that permit some air to pass though the septa from alveolus to alveolus promoting collateral ventilation and even distribution of air among the alveoli
1134
***Canal of lambert
NOT IN BOOK (mentioned in slides but not defined)
tiny canals that connect the distal bronchiolar tree to the alveoli
similar to pores of kohn but different structures
lecture & our friend chat!
What is surfactant?
What makes it?
a lipoprotein that cotes the inner surface of the alveolus and facilitates its expansion during inspiration by lowering alveolar surface tension. At end expiration prevents lung collapse
–also plays a role in infection defense
Made by Type 2 alveolar cells
1134
What is the pleura?
What are the two types?
Why is the pleura so important?
A serous membrane that adheres firmly to the lung and then folds over itself and attaches firmly to the chest wall. Usually contains a small amount of pleural fluid to lubricate the surfaces allowing the surfaces to slide over each other without separating.
Visceral pleura: covers the lungs
Parietal pleura: covers the thoracic cavity
Has a negative pressure required for the lung to expand on inspiration
1137
**What is transpulmonary pressure?
pressure difference between pleural and alveolar pressures
Maintain airway patency during respiration
lecture and organizer
**What keeps lungs from collapse at the end of exhalation?
PEEP
Surfactant
Closed Glottis
lecture
What is lung compliance?
What is it determined by?
degree lungs expand per unit of change in transpulmonary pressure. A measure of lung and chest wall distensibility and is defined as volume change per unit of pressure change.
It represents the relative ease with which these structures can be stretched and is therefore the opposite of elasticity.
Determined by:
Alveolar surface tension and elastic recoil of the lung and chest wall.
Compliance= change in volume/change in pressure
1142
Why is surface tension elastic force?
air fluid interface creates a force that cause alveoli to collapse inward, this is countered by surfactant which facilitates expansion during inspiration
–influential in lung volume management during breathing, especially in conditions like PEEP, with surfactant.
1134
**What is different between the child thoracic cage and compliance compared to the adult?
Children have cartilaginous ribs, making the chest wall less rigid and easier to expand but also has strong recoil and more potential for collapse during exhalation.
Adults especially as we age decrease elastic recoil
Lecture
What conditions increase the work of breathing?
Decreased lung compliance- pulmonary edema/fibrosis
Decreased chest wall compliance- scoliosis or obesity
Airway obstruction- bronchospasm or mucous plugging
1142-1143
What is inspiratory reserve volume (IRV)?
maximum extra volume of air that can be inspired after a normal tidal volume
aka
deepest breath possible volume - normal volume inhaled
DECREASE OBSTRUCTIVE LUNG DISEASE
~3L
1148 chart
What is expiratory reserve volume (ERV)?
maximum extra volume of air that can be expired at the end of a normal tidal volume.
aka
maximum exhaled volume - normal volume exhaled
DECREASED ASTHMA OR COPD (obstruction)
~1200mL
1148 chart
What is residual volume (RV)?
The volume of air that remains in the lungs at the end of a forceful exhalation.
INCREASED WITH COPD/EMPHASEMA
~122mL
1148 chart & 1144
***What is inspiratory capacity (IC)?
tidal volume + inspiratory reserve volume
max air that can be inhaled after a normal expiration
DECREASED IN RESTRICTIVE AIRWAY DISEASE, can be normal if not in acute exacerbation
~3500mL
organizer
What is functional residual capacity (FRC)?
expiratory reserve volume + residual volume
the volume of air remaining in the lungs after a normal exhalation
INCREASED OBSTRUCTIVE LUNG DISEASE
DECREASED RESTRICTIVE LUNG DISEASE
1149
What is Vital capacity (VC)?
inspiratory reserve volume + tidal volume + expiratory reserve volume
the maximum volume that can be exhaled after a maximum inhale.
the maximum amount of air that can enter and leave the lungs during respiration
DECREASE RESTRICTIVE LUNG
NORMAL OR INCREASED OBSTRUCTIVE
~2400mL
1148
What is total lung capacity (TLC)?
Inspiratory reserve+ tidal volume+ expiratory reserve+ residual volume
maximum volume the lungs can be expanded.
INCREASED OBSTRUCTIVE
DECREASED RESTRICTIVE
~6L
1149
What are the two clinically significant pulmonary function tests?
What do they tell you?
Forced vital capacity (FVC)
Forced expiratory volume in 1 second (FEV1)
————FEV1/FVC Ratio
Early detection of of restrictive or obstructive deficits, severity classification, monitoring progression
Restrictive lung diseases restrict volume; the lungs are unable to expand normally diminishing the amount of gas that can be inspired therefore reducing the FVC.
Obstructive disease affects gas flow; airflow into and out of the lungs is obstructed reducing the FEV1
Ratio: Diagnostic tool
RESTRICTIVE DISEASE: FVC DECREASED
OBSTRUCTIVE DISEASE: FEV1 DECREASED
1148
What is forced vital capacity (FVC)?
maximum amount of air that can be displaced from the lung during a forced expiration.
1149
What is minute ventilation?
Clinical Significance?
Rate of ventilations/min x the volume or amount of air per breath in L= _____L/min
OR
Tidal volume x ventilation rate
the total amount of air moved into the lungs each minute
Clinical significance:
-Key indicator how well lungs are functioning
-Hypoxia/hypercapnia monitoring: can indicate gas exchange issue (hypoventilation leading to hypoxia or hypercapnia)
1137
What is alveolar ventilation?
Why don’t we use that measure at the bedside?
rate new air reaches the gas exchange areas of the lungs
the rate can not be accurately determined by observation of rate, pattern, or effort. If adequacy of ventilation needs to be determined ABG or capnography must be used to determine if there is CO2 retention.
1138
What is dead space ventilation?
Why don’t you want it?
There are two main kinds, what are they?
-The volume of air per breath that does not participate in gas exchange. It is ventilation without perfusion.
-on exhalation the air in the dead spaces is expired first before air from the alveoli which decreases CO2 removal. Diseases causing dead space make CO2 harder to blow off (COPD/asthma)
Anatomic dead space= volume of air in the conducting airways (no gas exchange) about 30% of tidal volume
Alveolar dead space= volume of air in unperfused alveoli
1138
**What is physiologic dead space?
What condition is it associated with?
Physiologic dead space = anatomic dead space + alveolar dead space
PNA, PE
lecture and organizer
What is the hila of each lung?
a wedge-shaped depression in the center of each lung where the bronchi, arteries, veins, and nerves enter and exit the lungs. The hilum is located in the mediastinal surface of the lung, in front of the 5th through 7th thoracic vertebrae.
1133*
What is the function of bronchial vessles?
provide oxygenated blood from the systemic circulation to: moisten inspired air and supply nutrients to the conducting airways, large pulmonary vessels, lymph nodes, and membranes (pleura), that surround the lungs.
1136
What is the alveolocapillary membrane?
Why is it so important?
very thin membrane made up of the alveolar epithelium, the alveolar basement membrane, an interstitial space, the capillary basement membrane and the capillary endothelium.
Gas exchange occurs across this membrane. The extremely thin alveolar walls are easily damaged and can leak plasma and blood into the alveolar space. Any disorder that thickens the membrane impairs gas exchange.
1136
Not in lecture but super important
What is hypoxic pulmonary vasoconstriction response?
Why does this happen?
A reaction to a low alveolar partial pressure of O2 (PaO2) causing increased pulmonary vascular resistance in the lung area (can be unit, lobe etc.) that is not well ventilated, causing a shunting of pulmonary blood flow to areas of the lung that are adequately ventilated therefore have a normal PaO2.
Attempt to maximize ventilation/Perfusion and avoid mismatch.
1137
What is V/Q mismatch?
What conditions cause it?
Alteration of ventilation(V)/perfusion(Q) ratio
An imbalance in the alveolar ventilation and the alveolar blood flow.
Normal: 0.8-1
Most common cause of hypoxemia
Asthma, chronic bronchitis, PNA, atelectasis, pulmonary embolism
1145-1146
What is the respiratory quotient?
Ventilation/perfusion= V/Q= 0.8 normal
represents the amount by which perfusion exceeds ventilation under normal conditions
1146
**What is physiologic shunting?
V/Q below normal –> inadequate ventilation to oxygenate blood flowing through alveolar capillaries
V/Q < NORMAL
organizer/lecture
From Google:
a type of blood recirculation that occurs when blood bypasses the pulmonary circulation and mixes with deoxygenated blood in the systemic circulation
A small amount of physiologic shunting is normal and is caused by vessels that supply the bronchi. However, shunting can also be caused by disease in the heart, pulmonary vasculature, or alveolar air space.
A key characteristic of shunting is that it doesn’t respond to supplemental oxygen. This is because the supplemental oxygen can’t reach the blood that has already bypassed the alveoli
Why do you put the good lung down?
dependent regions of the lung get more blood flow due to compression of capillaries in the low pressure areas. Changing positions changes flow distribution.
example: a person standing has less blood flow to the apices than the lower lobes.
1146
How do blood flow zones work?
And not work?
Works in all areas of the lung, depending on positioning. zone 3 (best) blood flow in all or most of lungs during exercise due to increased cardiac output.
doesn’t work: zone 1 blood flow (worst) occurs when PA pressures are too high (pulmonary HTN), or alveolar pressures are too high (hyperinflation-> asthma/COPD), or in the least dependent area of the lung at any given time.
Seriously a picture is much easier to understand!
1146 Fig 34.05
Mostly slide
What is the Bohr effect?
shift in the oxyhemoglobin dissociation curve cased by changes in the CO2 and hydrogen ion concentrations in the blood.
1147
What is the Haldane effect?
the property of hemoglobin that allows it to carry more carbon dioxide (CO2) when it’s deoxygenated than when it’s oxygenated
1148
What is Mean filtration pressure?
net fluid movement from alveoli to interstitial space that drains into the lymphatic system.
Helps prevent pulmonary edema.
Book??
According to Google:
Pulmonary capillary pressure (Pcap) is the average hydrostatic pressure in the small pulmonary vessels where filtration occurs. It’s the filtration point in the capillary bed and determines how much interstitial fluid builds up in the lung
Definition of pulmonary edema?
Why do we care?
excessive fluid in alveoli due to a failure of one of the clearing mechanisms:
-lymphatic drainage, capillary hydrostatic pressure, capillary oncotic pressure, and capillary permeability.
impedes gas exchange
1165
Common causes (and the most common cause) of pulmonary edema?
MOST: Left sided heart disease
pulmonary over-circulation
Increased pulmonary capillary permeability (inflammation, ARDS, or inhalation of toxic gases)
Obstruction of the lymphatic system
1165
Clinical manifestations of pulmonary edema and assessment findings?
Dyspnea
tissue hypoxia
increased WOB
Crackles, pink frothy sputum
1166
What is pleural effusion?
What are the types (5)?
Excess fluid in the pleural space
- Transudative
- Exudative
- Empyema
- Hemothorax
- Chylothorax: tear in the thoracic duct leading to the leakage of chyle (lymph formed in the GI system) into the pleural space. (rare complication of surgery and some malignancies)
What is transudative pleural effusion?
Transudative: clear or slightly discolored, contain few cells and little protein.
1160
What is exudative pleural effusion?
Exudative: response to inflammation, infection or malignancy. Leukocytes and plasma proteins migrate out into affected tissue. Parapneumonic effusions (PNA)
1160
What is empyema?
Empyema: contains infectious microorganisms
1160
What is hemothorax? How?
Hemothorax: blood (trauma, surgery, cancer, PE or TB)
1160
What is chylothorax?
Chylothorax: tear in the thoracic duct leading to the leakage of chyle (lymph formed in the GI system) into the pleural space (rare complication of surgery and some malignancies)
1160
What is SpO2? OR SaO2 in the book?
Percent of Hgb saturated with O2 in arterial blood
Normal 97-100
1145 34.2
What is SvO2?
Percent Hbg saturated with O2 in mixed venous blood
Normal 75
1145 34.2
Oxyhemoglobin dissociation curve shift to the RIGHT
Acidosis, increased CO2, Increased Temp, Increased DPG
decreased affinity of Hbg for O2, O2 readily released in tissue
More common for a right shift
Oxyhemoglobin dissociation curve shift to the LEFT
Alkalosis, decreased CO2, decreased temp, decreased DPG
increased affinity of Hgb for O2, Less O2 to tissues
Less common
Where is the respiratory center in the brain?
Medulla oblongata and pons
Medulla:
–Dorsal - inspiration
–Ventral- expiration
Pons: pneumotaxic center- controls rate and pattern
1138
How do dorsal respiratory neurons affect breathing?
Rate and inspiration time
Vagal and glossopharyngeal nerves
Chemoreceptors and baroreceptors
Diaphragm and intercostal muscles
1138
How do ventral respiratory neurons affect breathing?
Basic rhythm
Diaphragm & intercostals
1138
Where are the central chemoreceptors that trigger breathing?
How do they work?
Medulla
Sense change in pH or CSF as CO2 crosses the BBB. As pH decreases they stimulate the respiratory center to increase the depth and rate of ventilation.
Become insensitive to small changes in CO2 with CO2 retaining pathology like COPD.
1139
Where are the peripheral chemoreceptors that trigger breathing?
How do they work?
Carotid and aortic bodies
senses changes in O2 concentration. lower PO2 increases respiratory rate.
Accompanied by dyspnea
1138
What is the Hering-Breuer Reflex?
aka the Hering-Breuer EXPIRATORY reflex
stretch receptors in the smooth muscle are sensitive to the increases in size or volume of the lungs. When stimulated they decrease the ventilitory rate and volume
NOTE: this reflex is active in newborns and assists with ventilation.
In adults it’s only active at high tidal volumes such as exercise and mechanical ventilation, may protect against excess lung inflation
1140
What do pulmonary C-fiber receptors (aka J-receptors) do?
Where are they located?
receptors sensitive to increased pulmonary capillary pressure, which stimulates them to initiate rapid, shallow breathing; laryngeal constriction on expiration; mucus secretion; hypotension; and bradycardia.
Associated with dyspnea
Located: near the capillaries in the alveolar septa and other airway locations as nociceptors.
1140
What is a pulmonary embolism?
What are the symptoms?
Full or partial occlusion of the pulmonary artery.
-Clot/DVT (venous thromboembolism)
-Fat
-Amniotic fluid
-Air
NOTE: 25% of people with PE will have the first symptom as sudden death
Symptoms:
Tachypnea
Dyspnea
Chest pain
Low Sat
1179
How is a pulmonary embolism diagnosed?
How is it treated?
Diagnosis:
-CTA/MRA (GOLD STANDARD HAHA!)
-D-dimer
-ABG (evaluate for hypoxemia)
-BNP & Troponin (markers for R ventricular dysfunction)
-EKG (look for R heart strain)
Treatment:
-Anticoagulation therapy if stable
–Xa inhibitors or lovenox
If unstable:
-IV fibrinolytic
-Catheter directed therapy (EKOS??)
-Thrombectomy
1180
What is the pathophysiology of Pulmonary Embolism?
Occlusion causes –>
-Hypoxic vasoconstriction
-Decreased surfactant
-Release of neurohumoral and inflammatory substances
-Pulmonary edema
-Atelectasis
1180
What is pulmonary hypertension?
What causes it?
Of those what is the most common cause?
Pressures in the PA > 25 at rest
Causes: 5 main categories with many subcategories
- idiopathic, heritable, drug and toxin, connective tissue disease
- Left sided heart disease
- lung diseases and/or hypoxia
- chronic thromboembolic
- unclear multifactorial mechanism (tumors, metabolic disorder, renal failure etc.)
–Not sure what category to put these but slides say chronic hypoxia, and valve disease
MOST common: Left sided heart failure
1181
What are the symptoms of Pulmonary hypertension?
Assessment findings?
How is it diagnosed?
Symptoms:
-May be asymptomatic until late in the disease process
-Fatigue
-Chest pain
-tachypnea
-dyspnea (especially with exertion)
-cyanosis
-syncopy
Assessment findings:
-peripheral edema
-JVD
-precordial heave
-accentuation of the pulmonary component of the second heart sound (???)
-Kidney problems
-Liver congestion
Diagnosis:
-CXR (usually first indication) showing enlarged R heart
-EKG with right ventricular hypertrophy
-CT
What is the pathophysiology of pulmonary hypertension?
How do we treat it?
Patho: endothelial disfunction with overproduction of vasoconstrictors (thromboxane & endothelin) and decrease in production of vasodilators (prostacyclin & nitric oxide) –> resistance to flow increases R heart strain causing hypertrophy –> cor pulmonale (right ventricular hypertrophy, dilation or both)
Treatment:
- O2 (treat underlying disease process)
- Diuretics
- Anticoagulants
- Avoid contributing factors (air travel, decongestants, NSAIDS, pregnancy, tobacco etc)
-Vasodilators (calcium channel blockers, inhaled nitric oxide)
-Refractory to treatment may need lung transplant
1181
What are the overarching symptoms of obstructive lung diseases?
- Dyspnea
- Wheezing (lower airway)
- Stridor (upper airway)
- Prolonged expiration (long FEV1)
1167
What is the pathophysiology of Asthma?
Early and Late response
Early:
-Exposure to an antigen causes a major immune response with HISTAMINE, LEUKOTRINES, CYTOKINE, CHEMOKINE, PROSTAGLANDIN, IgE, PLATELET ACTIVATING FACTOR, TRYPTASE AND CHYMASE
-Mucosal edema and mucus production increases
-Bronchospasm, THROMBOXANES increased contractile response of bronchial smooth muscle.
Late:
-4-8 hours after exposure
-Chemotactic recruitment of eosinophils (and friends) release more inflammatory mediators restarting the inflammatory response
—-causing mucosal edema, mucus production, bronchospasm, contractility of smooth muscle
If untreated long term inflammation causes airway damage and airway remodeling that becomes permanent
INCREASED RV, FRC AND TLC
NORMAL OR DECREASED VC AND IRV
1170
Causes of Asthma
Familial or environmental. More commonly familial
Can also be indoor or outdoor pollution, tobacco, obesity, GERD etc.
Occurs at all ages, more common in women and those below the poverty level
1167
What are the symptoms and treatment of asthma?
Symptoms:
-asymptomatic between attacks, pulm function tests are normal.
-chest constriction
-expiratory wheezing
-dyspnea
-nonproductive cough
-prolonged expiration
-use of accessory muscles
-Tachycardia
-tachypnea
Treatment:
-Avoid allergens and irritants
-inhaled low dose corticosteroids (pulmicort)
-Beta 2 agonists (albuterol) - should only be used when necessary is associated with increased risk for severe exacerbations
-Anticholinergic stimulators (Ellipta or atrovent)
-Antihistamine (zyrtec etc.)
-Antileukotrienes (singulair)
-Steroids
1171-1172
COPD causes?
Typically acquired
Genetic: alpha1-antitrypsin deficiency, more common in those with European descent and results in early age COPD without smoking.
Most common lung disease in the world
INCREASED RV, FRC AND TLC
NORMAL OR DECREASED VC AND IRV
1173
What is Chronic bronchitis?
Hypersecretion of mucus and chronic productive cough that continues at least 3 months of the year, and for at least 2 consecutive years.
1173
What is the pathophysiology of chronic bronchitis?
-Bronchial inflammation caused by inspired irritants causing edema—>
-Increased size and number or mucous glands and goblet cells –>
-smooth muscle hypertrophy with fibrosis and narrowing of airways–>
-Thick tenacious mucus is produced and cannot be cleared because of impaired ciliary function compromising defense mechanisms, and air trapping
1173
What are symptoms of chronic bronchitis?
Symptoms:
-Dyspnea on exertion (eventually as it gets worse marked dyspnea even at rest)
-persistent productive cough
-Wheezing
-Barrel chest
-cyanosis
-hypoxemia
-polycythemia
-cor pulmonale
-CO2
-V/Q mismatch
-Chronic hypercarbia
(blue bloaters- obese, cough, cyanosis)
1173
What is the pathophysiology of emphasema?
Destruction of alveolar walls results in permanent enlargement of gas exchange airways. (large alveoli instead of smaller ones with more surface area for gas exchange)
-Obstruction results from inflammatory changes
-inflammation and imbalance in proteases and antiproteases, oxidative stress and apoptosis of lung structural cells
-destruction of alveoli produces large air spaces within the lung (BULLAE) and air spaces adjacent to pleurae (BLEBS)
——V/Q mismatch and hypoxia
–Malnutrition
-no mucous like chronic bronchitis
(pink puffers- pink skinny)
1173
What is emphaysema?
Abnormal, permanent enlargement of gas exchange airways (acini) accompanied by destruction of alveolar walls without obvious fibrosis.
Associated with enhanced chronic inflammatory response in airway to noxious particles or gases.
1173
What is croup?
Symptoms?
Treatment?
obstruction of the upper airway in children, subglottic edema causing narrowing of airway and respiratory distress
6mo- 3yrs
Symptoms:
-barky cough
-inspiratory stridor
Treatment:
-oral or inhaled glucocorticoids
-nebulized epi
-rarely intubation
-supportive care
Not common thanks to vaccination (diphtheria, RSV, rhinovirus, adenovirus, rubella)
USUALLY RESOLVES IN 3-7 DAYS
1191
What is Acute epiglottitis?
Symptoms?
Treatment?
Usually affects children 2-6 caused by H. influenzae type B (HiB).
-life threatening edema of the epiglottis possibly causing obstruction of the upper airway
Symptoms:
-inspiratory stridor
-sudden development of high fever
-severe respiratory distress
-drooling
-tripod
Treatment:
-Keep them calm
-Intubation
-broad spectrum abx & corticosteroids
Not common thanks to vaccination, increasingly an issue for adults now. :(
1193-1194
What is cystic fibrosis?
Symptoms?
Treatment?
-autosomal recessive genetic disorder, defective epithelial chloride ion transport (CFTR gene)
-Multiorgan (lungs, GI & reproductive) disease
-chloride and water are not transported appropriately across epithelial membranes. Chronic inflammation with excessive cytokines and neutrophils
Symptoms:
-thick dehydrated mucus secretions (mucus plugging)
-persistent cough or wheeze
-excessive sputum production
-recurrent or severe PNA
-chronic sinusitis
-malnutrition
-intestinal obstruction
-eventually barrel chest and digital clubbing
Recurrent Infections:
-Pseudomonas most common
-PNA bacterial, fungal and viral
Treatment:
-Chest cpt
-pancreatic enzymes
-bronchodilators
-hypertonic saline inhalation (break up secretions)
-High dose NSAID > 6 yrs old. (emerging)
1205-1206
What is restrictive airway disease?
What are examples?
decreased compliance (stiffness) of lung tissue, resulting in increased WOB to expand lungs during inspiration
Examples:
-Scoliosis
-muscular dystrophy
-morbid obesity
-aspiration
-atelectasis
-bronchiectasis
-pulmonary fibrosis
-pulmonary edema
-ARDS
-bronchiolitis
TYPICALLY DECREASED VC, IC, FRC, AND TLC
NORMAL OR DECREASED RV
NORMAL FEV1/FVC
1161
What is bronchiolitis?
diffuse injury of the bronchioles resulting in inflammation and fibrosis. Primary usually in children due to viral infection. Adults smoking (asbestos/coal) and chronic bronchitis, pulmonary fibrosis but can be in healthy people.
Symptoms:
-hypoxemia
-decreased minute ventilation (increased accessory muscle use)
-hypercarbia
-tachypnea
-nonproductive cough
1163
What is pulmonary fibrosis?
Causes?
excessive amount of fibrosis or connective tissue in the lung.
-chronic inflammation
-fibrosis around the alveoli (stiffness), myofibroblast proliferation, causes decreased oxygen diffusion and hypoxemia.
-progressive increase in WOB as compliance decreases
-hypoventilation and hypercapnia
-idiopathic, ARDS/TB, RA/sarcoidosis, coal/asbestos
1163
How is respiratory failure defined?
What are the two subtypes and their definition?
inadequate gas exchange. Generally a result of direct injury to lungs, airways or chest wall; or indirectly because of disease or injury involving another body system (brain/spine/heart).
Hypoxemic PaO2 <60 (<50 on the slides)
Hypercapnic/Hypercarbia PaCO2> 50 AND pH < 7.25
1158
Difference between Hypoxemic and hypercapnic respiratory failure?
Hypoxemic:
-low PaO2 (slides with or without hypoxia?)
-inadequate O2 exchange between alveoli and capillaries
-tachycardia, cyanosis, confusion
–Give O2!
———-(slides: heart failure, increased alveolar membrane thickness, hypoventilation)
Hypercapnic
-high CO2
-inadequate alveolar minute ventilation (hypoventilation)
-confusion & lethargy
–Ventilatory support! Bipap, bag mask, vent/intubation
———(slides: neuromuscular disease, airway obstruction, physiologic dead space, chest wall deformity)
1158
**What is the P/F ratio?
What does it tell you?
PaO2/FiO2
Assesses for the severity of hypoxemic respiratory failure.
MUST be only part of the evaluation
-active inflammatory process
-acute (<7 days)
-resp failure not from cardiac cause or overload
Acute Lung Injury </or equal to 300
ARDS </or equal to 200
ONLY SLIDES
**What are the three phases of Acute lung injury?
Exudative Phase- inflammatory stage where fluid/edema builds up in alveoli preventing gas exchange
Proliferative Phase- early signs of healing. edema beings to drain (lymphatic) may have increased pleural effusions, pulm edema improves. Capillary alveolar barrier begins to restore.
Fibrotic Phase- Does NOT always occur, but very likely with ARDS at least in some part. Can have interstitial or capillary fibrosis as well. Risk for pulm HTN.
Lecture
External vs Internal Respiration
External: lungs and environment
Internal: blood and cells
Organizer
What is Fick’s Law?
The rate of diffusion is influence by surface area, thickness or alveolar membrane and the partial pressure gradients of gasses.
Organizer
What structures are part of the conducting airways?
Nose
Pharynx
Larynx
Trachea
Bronchi
Bronchioles
1131-1132
What structures are part of the respiratory zone?
Terminal bronchioles
Alveoli
Alveolar capillaries
1133-1134
What is Poiseuille’s Law?
resistance is directly related to tube length and blood viscosity, and inversely related to the radius of the tube to the 4th power.
1043
Works for airways too. The smaller the tube the higher to the 4th power the resistance.
lecture and organizer
Alveolar pressure changes during ventilation?
Starts at 0
drops below atmospheric pressure during inspiration
rises above atmospheric pressure during exhalation
lecture & organizer
What is the acinus?
A cluster or respiratory bronchioles, alveolar ducts and alveoli, DISTAL to a single terminal bronchiole
1133
Old age related changes in the respiratory system?
-Alveoli- loss of wall tissue & enlargement decreasing the surface area for diffusion, increased stiffness
Pulmonary capillaries- decrease in number and complexity of alveolar capillaries.
-Chest wall- decreased compliance and elastic recoil, reducing respiratory reserve, decreased strength, postural changes
-Vital capacity decreases and residual volume increases without a change in total lung volume
-Aging can cause the PaO2 to decrease but does not affect CO2
—-Results in increased risk for PNA, COPD & other resp infections
1151 & organizer
What is A-a gradient
Alveolar- arterial gradient
lecture & organizer
Google:
a measurement of the difference in oxygen concentration between the alveoli and the arterial system. It’s a useful tool for diagnosing hypoxemia and determining its severity
Primary Spontaneous Pneumothorax (PSP) vs
Secondary Spontaneous Pneumothorax (SSP) vs
Traumatic Pneumothorax vs
Tension Pneumothorax
PSP
-No apparent cause or lung disease (usually young males 20-40) caused by spontaneous rupture of blebs on the visceral pleura, possible genetic component
SSP
-Pre-existing lung disease which integrity of the visceral pleura is compromised.
Traumatic
-punctures by fractured rib or knife/bullet wounds, or iatrogenic (caused by medical procedure) such as needle aspiration, mechanical ventilation (barotrauma). Frequently involves BOTH visceral and parietal pleura
Tension
-site of pleural rupture acts as a one way valve, permitting air to enter the pleural space on inspiration but preventing escape during expiration. More air enters pleural space the pushes against the lung, causing compression atelectasis, mediastinal shift, severe respiratory distress, hypotension, and eventually death.
1159
Risk factors for PTX
-Young adult (15-34)
-Lung disease
-Tall/Thin (esp males and esp PSP)
-Hx of PTX
-Smokers
-Having invasive medical procedures (central line/thora/biopsy etc)
-Trauma
Organizer
Symptoms & treatment of PTX
-Sudden pleural pain
-Tachypnea
-Dyspnea
-decreased breath sounds
-hyperresonance
-severe hypoxemia (tension)
-tracheal deviation away from affected lung (tension)
-hypotension (tension)
Treatment:
-One way chest valve (PSP)
-Aspiration/chest tube with water seal and suction
-Surgery
1159
What is tidal volume?
volume of air inhaled or exhaled with each normal breath
RESTRICTIVE LUNG DISEASE ISSUE
~500 mL
FEV1/FVC ratio
Normal value
Obstructive Lung Disease Value
Restrictive Lung Disease Value
Ratio often seen as percent
Normal 70-80% (0.7-0.8) varies based on age, size etc.
Obstructive: <70% (COPD/Asthma)
Restrictive: >75% (Pulm fibrosis, Pna)
Notes:
Obstructive Severity Scoring
——Mild FEV1>80%
——Moderate FEV1 50-79%
——Severe FEV1 <50%
Organizer
Difference in child and adult airway/chest wall and alveoli
Adult:
-Normal Epiglottal movement
-More rigid/less space for expansion, other contributing factors such as obesity
Child/Infant:
-Hypoactive epiglottal movement (risk for aspiration)
-More compliant airways/smaller airways can collapse due to easy recoil
-Particularly vulnerable to airway obstruction
organizer
Blood flow zones 1-3
Zone 1: Dead Space
—alveolar pressure exceeds arterial pressure causing little to no blood flow in pulm capillaries. Normal, worse with things like hypotension.
Zone 2: Fluid Exchange
—arterial pressure exceeds alveolar pressure allowing pulsatile flow. Favorable for gas exchange.
Zone 3: Optimal Gas Exchange
—both arterial and venous pressures exceed alveolar pressure leading to continuous flow. Ideal for gas exchange as blood flow is constant allowing for continuous exchange.
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Acute Lung Injury
Causes
Diagnosis
Features
PEEP
occurs when the lungs are suddenly damaged, leading to inflammation, fluid accumulation in alveoli, and impaired oxygen exchange. Alveolar capillary membrane injury, inflammation and endothelial dysfunction
(considered a less severe version of ARDS)
Cause:
-Pna
-Aspiration
-toxic inhalation
-pulmonary edema
-sepsis
-trauma
-pancreatitis
Diagnosis:
P:F ratio- PaO2/FiO2 ratio of 200-300mmHg
Features:
-lung injury
-pulmonary edema
-inflammation
-compensatory mechanisms may function for a period
-cyanosis
PEEP:
Moderate PEEP, should improve oxygenation without hemodynamic compromise
organizer
ARDS
Causes
Diagnosis
Features
PEEP
the more advanced, critical stage of lung injury
Causes:
-PNA
-Aspiration
-Toxic inhalation
-Sepsis
-TRALI
-Severe pancreatitis
Diagnosis:
P:F ratio- PaO2/FiO2 ratio < 200mmHg
Features:
-Severe pulmonary edema
-widespread atelectasis
-decreased lung compliance
-severe hypoxemia
-diffuse alveolar damage
PEEP:
HIGH PEEP, watch for decreased cardiac output from decrease in venous return…. also PTX but they don’t seem to care about that one HAHAHAHA!
What is Central Hypoventilation Syndrome?
Rare disorder in which the automatic control of breathing is impaired, particularly during sleep. People with this condition fail to breathe normally because the brain’s autonomic centers do not properly respond to hypoxemia or hypercapnia levels in the blood, especially during sleep when breathing is largely under involuntary control
Can be congenital (genetic mutation) see in infants or in early childhood
Can be acquired due to brainstem injury, trauma, stroke, tumors, MS or post infection autoimmune response
