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
