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151 Cards in this Set

  • Front
  • Back
Completely removed in respiration
PGE1
PGE2
F2 alpha
Leukotrienes
Not effected by respiration
PGA1
PGA2
PGI2
Epi
Isoproterenol
Dopamine
ANG II
85%-90% removed in respiration
5HT
30% removed in respiration
Norepinephrine
80% removed in respiration
Bradykinin
70% converted in respiration
70% of ANG I converted to ANG II
40%-50% removed in respiration
ATP and AMP
Removed in plasma in respiration
Acetylcholine
Functions of Respiration
gas exchange
acid-base balance (carbonic anhydrase)
phonation (speech - air over vocal cords)
control temp/humidity
pulmonary defence mechanisms
pulmonary metabolism
Pulmonary Defense Mechanisms
ciliated epi
mucociliary elevator
mucus
cough reflex
turbulent precipitation
Speed of Laminar Flow
Fastest in the middle
Volume and pressure change during contraction
Increase volume in thoracic cavity

Decrease pressure in lung
If negative pressure inside and positive pressure outside, where will air flow?
It will flow in
Number of generations in bronchial tree
23
2 zones in bronchial tree
Conducting zone

Transitional/Respiratory Zones
Conducting Zone
150mL air
No gas exchange
Generations 1-16
Trachea - bronchi - bronchioles - terminal bronchioles
Diameter, Length, Number, area in conducting zone
Diameter: Decreases
Length: Decreases
Number: Increases
Area: Decreases from trachea to bronchioles. Increases from bronchioles to terminal bronchioles
Transitional/Respiratory Zone (AKA Acini)
350mL air
gas exchange
Generations 17-23
Respiratory bronchioles to alveolar ducts to alveolar sacs
Diameter, Length, Number, and area in Acini
Diameter: Decreases
Length: Decreases
Number: Increases
Area: Increases
Number of alveoli in adults

Surface area for gas exchange
300-480 million - avg is 300

50-100m^2 for gas exchange
Capillaries in bronchial tree
280 billion capillaries cover the alveoli
500-1000 cap/alveolus
Distance of terminal bronchioles to most distant alveolus
5mm
Primary Bronchi
generation 1, enter lung at Hilus
Segmental Bronchi
generation 3
Bronchioles
generation 4-16
Terminal Bronchioles
generation 16
Conduction Airways
nose to terminal bronchioles – anatomical dead space
Respiratory Bronchioles
have alveoli budding off

generations 17-19

transition
Alveolar Ducts
completely lined with alveoli

generations 20-22
Alveolar Sacs
groups of alveoli

generation 23
Barriers to get blood across
Alveolar Epithelial Cells
Interstitial Space
Capillary Endothelial cells
Erythrocyte - combine w/ hemoglobin
Time for gas exchange in capillaries
Normal breathing: 3/4 s

Fast breathing: 1/4 s
What is very important in bronchiolar structure?
Tone

EX: asthma is over sensitive smooth muscle response
Receptors for asthma
B2: albuterol on bronchial smooth muscle and relax it

Muscarinic: (ACH) receptors that contract
Structure of tissue on bronchus
mucous blanket
cilia
goblet cells
epi
smooth muscle
mucous gland
submucosal ct
cartliage
Structure of tissue in bronchiole
cilia
goblet cells
epi
smooth muscle
sumucosal ct
Structure of tissue in alveolus
.
Type 1 Pneumocyte
thin squamous cells flattened nucleus
95 % of surface area of alveoli
Type 2 Pneumocyte
cuboidal shaped cells located at corners of alveoli
5% of surface area, synthesize surfactant and precursor of type I cells
Alveoli
Thin walled polyhedral sacs

2 to 6 X 108 average 300 million

0.25 to 0.33 mm in diameter

Surface area 50-100 m2
Dense capillary bed 280 billion
capillaries 500-1000 per alveoli ~ 70 m2
Blood-Gas Barriers
1. Surfactant
2. Alveolar epithelium type I and II pneumocytes
3.Interstitial space – fluid filled basement membrane
4.Capillary endothelium
5.Plasma
6.Erythrocyte membrane
Tidal Volume
volume expired or inhaled with each normal breath ~ 500 mls
Inspiratory Reserve Volume
volume that can be inspired after a normal tidal
volume ~ 3100 mls
Expiratory Reserve Volume
volume forcefully exhaled after a normal tidal
volume ~ 1200 mls
Residual Volume
volume remaining in the lungs after forceful exhalation
~ 1200 mls
Inspiratory capacity
Inspired reserve volume plus tidal volume
~ 3600 mls
Vital capacity
Maximum amount of air that can be expired following maximum filling of lungs
~ 4800 mls
Total lung capacity
maximum volume of lung expansion
~ 6000 mls
Functional Residual Capacity (FRC)
the volume of air in the lungs at the equilibrium position (no active muscle contraction) elastic recoil forces of lung equal elastic recoil forces of chest wall. Resting end-expiratory position
~ 2400 mls. Can’t be measured by a spirometer
Minute respiratory volume
tidal volume X respiratory rate
~ 500 mls X 12/min = 6000 mls
minute alveolar ventilation
new air reaching gas exchange area of lungs ~ 500– 150 mls (anatomical dead space X respiratory rate = 350 X 12 = 4200 mls
Forced expiratory volume (FEV)
Inhalation from FRC to TLC ( about 1 sec to do) followed by forceful exhalation from TLC to RV ( about 5 sec to complete). Normal subjects exhale 80% of FVC in first second. FEV1 is diminished in patients with obstructive lung disease and increased in patients with restrictive disease lung disease
Negative Pressure Breathing
normal due to alveolar pressure
< atmospheric pressure
Positive Pressure Breathing
done by machines on patients that can’t ventilate properly atmospheric > alveolar pressure
Air Flow moves
Air like fluids moves from a region of higher pressure to lower pressure, therefore for air to move into and out of the lungs a pressure difference must exist between the alveoli and the atmosphere
Poiseuille's Law
F= ΔP/R
R equals
R = η x L x 8/π x r^4
Flow (V) equals
V = ΔP x π x r^4/η x L x 8
Boyle's Law
Pressure and volume are inversely related

Applies to diaphram contraction
pneumothorax
hole in lung
Alveolar Pressure Equals
Alveolar pressure = pressure inside of alveolar space, at rest equal to atmospheric pressure (760 mm Hg or 0 cm H20)
When does air flow out of the lungs?
Air flows out of lungs when alveolar pressure is sufficiently greater than atmospheric pressure to overcome the resistance of the airways
When does air flow into lungs?
Air flows into lungs when alveolar pressure less that atmospheric and can overcome resistance
Why do muscle of inspiration contract?
Muscle of inspiration contract to increase the volume of the alveoli lowering the alveolar pressure according to Boyle’s law (pressure and volume inversely proportional, as one doubles the other halves) as pressure decreases air flows inward.
What is intrapleural pressure equal to?
Intrapleural pressure = pressure in the thin space (10 -30 μm at normal lung volumes, 15-25 mls of fluid) between visceral and parietal pleura, is normally negative -3 to -5 cm H20.
Why is intrapleural pressure negative?
When all respiratory muscles are relaxed the lung tends to decrease its volume because of elastic recoil of the distended alveolar walls and the chest wall tends to increase its volume by outward elastic recoil. At FRC=2400 mls
Transmural Pressure Gradient (TMP) equals
TMP = alveolar pressure - intrapleural pressure
Principal of TMP
Chest wall is acting to hold alveoli open in opposition to elastic recoil, similarly the lung is acting by its elastic recoil to hold the chest wall in
How is the pressure gradient across the outermost alveoli transmitted?
The pressure gradient across the outermost alveoli is transmitted mechanically through the lung via the alveolar septa
Diaphragm
dome shaped muscle separates thorax from abdominal cavity, innervated by phrenic nerves which leave spinal cord at 3rd -5th cervical segments.
Movement of diaphragm during breathing
During quite breathing may descend 1-2 cm, during deep inspiration may descend 10 cm. Connected to 6 lower ribs, sternum and by two crura to spinal cord
Intercostal muscles during inspiration
External Intercostal
Intercostal muscles during expiration
Internal Intercostal
External Intercostals
external intercostals, scalene and parasternal intercostals and muscles raise and enlarge the rig cage.
Sternocleidomastoid muscle involved in labored breathing elevates sternum and helps increase anterior-posterior and transverse dimensions of chest. Often involved during asthma attacks.
Dyspnea
feeling of breathing difficulty may be caused by fatigue of inspiratory muscles
ACH and diaphragm
Nerve fibers activated by release of ACH on nicotinc receptors. Diaph contracts
Ca2+ - actin - myosin - tropomysin - back to SR to relax.
Expiration is what during normal quiet breathing?
Expiration passive during normal quite breathing. As inspiratory muscle relax the elastic recoil of alveoli are sufficient to decrease alveolar volume and raise alveolar per assure above atmospheric
Which muscles are involved in active respiration?
include muscles of abdominal wall:
rectus abdominis
external and internal oblique
transverse abdominis internal intercostals
Transpulmonary Pressure
Transpulmonary pressure = pressure in trachea – intrapleural pressure.
It is a measure of pressure difference across whole lung. At end of inspiration or expiration pressure = 0 cm H2O
Compliance Equals
Change vol/Change press
Compliance represents
the ease with which something can be stretched or distorted

It is the inverse of elasticity
Elasticity
Tendency to resist stretch or distension
Compliance and Isolated Lungs
where changes in lung volume were graphed against changes in pressure
Hysteresis
difference in curves: caused by surfactant, and recruitment of alveoli
Chest Muscles and Compliance
Chest muscles also show compliance

1/total compliance = 1/lung + 1/chest wall
Lung Compliance Circuit
Compliances in parallel add directly so compliance of two lungs is greater then either lung alone

- people with ↓ compliance of lungs must do more work to inspire than normal
- people with ↓ chest wall compliance must do more work than normal
(obese and other muscle problems moving chest and ribs upward)
Fibrosis
due to tissue damage makes lungs less compliant or stiffer, increase elastic recoil. Collapsed alveoli (atelectasis) also make the lung less compliant
Emphysema
due to loss of septal walls that oppose lung expansion make the lungs more compliant
Surface Tension Forces
Surface tension forces occur at any gas-liquid interface and are generated by cohesive forces of
the liquid molecules. Surface tension is what makes water droplets form spheres.
LaPlace's Law
P (dyn/cm) = 2 x T (dyn/cm)/r (cm)
T equals
P x r/2

T= tension on outside
P= press grad in h2o drop
r= radius of sphere inside h2o drop
Droplet size is determined by?
Droplet size is determined by point at which pressure of fluid inside droplet equals tension of droplet to collapse
How are 2 alveoli of diff size connected?
two alveoli of different sizes are connected by common airways and the surface tension is equal, the pressure of then smaller alveolus is greater than the larger one and will collapse and empty into the larger one
If surface tension is controlled...
the smaller alveoli will not collapse
Surfactant is made of
85-90% lipids and 10-15% proteins, 75% diplamitoyl phosphatidylcholine, 4 surfactant proteins SP-a, SP-B, SP-C and SP-D
Surfactant Production
Continuously produced by type II pneumocytes and taken back into type II cells to be degraded into other phospholipids
Functions of surfactant
stabilize alveoli, lower surface tension of smaller alveoli, increases compliance of lungs, decreases elastic recoil of lungs and decreases work of inspiration
Clinical Consequences of surfactant
fetal surfactant is not produce until about the 4th month and is not fully functional until 7th month or later, so premature infants have difficulty initially inflating lungs and keeping lungs inflate, leads to infant respiratory distress syndrome.
Treatment of mother
Give mother (Betamethasone Im 12 mg/24hrs/2 days, or Dexamethasone Im 6 mg/12 hrs/2 days) to induce formation in fetus during weeks 27-34 of gestation or use synthetic surfactant.
What can decrease surfactant?
Hypoxia or hypoxemia may decrease surfactant or increase breakdown and adult respiratory distress syndrome or Shock-lung seen after trauma or surgery)
Alveolar Interdependence
Alveoli are not spheres, they are interdependent polygons with shared walls. They are held open by the chest wall pulling on the outer surface of the lung.
How does alveolus respond to collapse?
If an alveolus tries to collapse it puts pressure on surrounding alveoli that will help keep it open
Surface Tension & the Interior and Exterior elastic Recoil
The inward elastic recoil of the lungs is opposed by the outward elastic recoil of the chest wall, when these forces are equal the volume of gas in the lungs is the Functional residual capacity (FRC)
What if the integrity of the lung-chest wall system is damage?
If a penetrating wound (knife, gsw): you loose intrapleural negative pressure, chest wall will move outwards due to elastic recoil and alveoli will collapse inward due to their elastic recoil and lungs will collapse.
Resistance and Change in pressure
Change in P = flow x resistance
Resistance in circuit
In Parallel: are added as reciprocals

In Series: Are additive
Pooseuille's Law Governs
movement of fluid through tubes
Change is Pressure is directly proportional to
Airflow (V) x Resistance (R)
F =
F = Change P/R
R =
.
Flow (V) =
.
When does turbulent flow occur?
Reynolds number above 2000
Re =
.
Airway Resistance
25-40 % of airway resistance in upper airways: nose, nasal turbinate's larynx, rest in generations 0-13 of bronchiolar tree (away from gas exchange)
What constricts bronchiolar smooth muscle?
-Parasympathetic nervous system (M3 receptors cholinergic receptors
-Acetylcholine
-Histamine (mast degran)
-Leukotriene's
-Thromboxane A2 (from PGA - activates platelets)
-Serotonin
-α1adrenergic agonists (small role)
-Decreased PCO2 in small airways (lots O2)
What relaxes bronchiolar smooth muscle?
-Sympathetic stimulation (β2 receptors)
-β2 agonists (regardless of what's cont it)
-Nitric oxide
-Increased CO2 in small airways
-Decreased PO2 in small airways
-M3 antagonist
Forced expiration and intrapleural pressure
During forced expiration intrapleural pressure may exceed intra-airway pressure which may increase resistance and may collapse the airway if the cartilaginous support or alveolar septal traction is insufficient. In patients with emphysema this can become a problem
How long does it take for FEV expiration?
In normal ind: 80% of FEV in 1st second.
Significantly longer if airway obstruction or collapse.
Airflow Volume Curves
Airflow-volume curves may be used to differentiate disease

Obstructive disease – limits airflow. ex: asthma, bronchitis and emphysema

Restrictive disease limits – lung expansion. ex: fibrosis, scoliosis,
Where do lungs receive blood from?
Lungs receive blood flow from both bronchial circulation (left heart) and pulmonary circulation
(right heart).
Pulmonary circulation is equal to 100% of output of right heart and equals left heart
Pulmonary Blood Flow At Rest
3.5 L/min/m2 at rest. Which is ~ 250-350 ml/m2 in pulmonary circulation. About 60-70 ml/m2 are in the pulmonary capillaries.
RBC's and pulmonary blood flow
It takes a red blood cell 4 - 5 seconds to travel through the pulmonary circulation and is in the pulmonary capillaries about ¾ sec in a person at rest. Pulmonary capillaries have a diameter of 6μm and red blood cell diameter is 8μm, therefore red blood cells have to change shape slightly to fit through.
Pulmonary Capillaries and alveoli for gas exchange
280 billion pulmonary capillaries supply 300 million alveoli so gas exchange area is 50-100 m2
Blood flows from the bronchial artery to?
The bronchiolar tree down to the level of the terminal bronchi receive blood flow from the bronchial artery
Structures distal to the terminal bronchioles received oxygen from?
respiratory bronchioles, alveolar ducts, alveolar sacs and alveoli receive oxygen directly by diffusion from the alveolar air and nutrients from mixed venous blood in the pulmonary circulation
Pulmonary Veins carry?

Pulmonary Arteries carry?
Pulmonary veins carry oxygenated blood

Pulmonary arteries carry low oxygen blood
Pulmonary Circulation Is
Pulmonary circulation is a low pressure system and is much thinner walled and more distensible and compressible than systemic circulation
Differences in Pulmonary Vessles
-Pulmonary vessels offer much less resistance to blood flow and work at much lower pressures.
-Pulmonary vessels are thinned wall which makes them much more distensible and compressible, because of this they are more affected by gravity, body position, lung volume, intrapleural pressure, and right
ventricular output
Alveolar Pulmonary Perfusion
As lung volume ↑, alveoli ↑ in volume stretch capillaries, ↑ length, ↓ diameter, increase resistance.
Extra Alveolar Pulmonary Perfusion
increased negative intrapleural pressure, stretches vessels to ↑ diameter, ↓ resistance
Positive Pressure Breathing
If positive end-expiratory pressure (peep) to prevent atelectasis, have ↑ alveolar pressure and ↑ intrapleural pressure can compress vessels and ↑ pressure. Can also compress venae
cava, and decrease venous return. (Edema)
During exercise when CO increases several fold, what happens to mean arterial pressure?
CO may inc several fold w/o a corresponding inc in mean arterial pressure unlike systemic circulation.
In isolated lung, as blood flow increases what happens to vasular resistance?
Vascular resistance will decrease.

Inc blood flow w/o working as hard. 2 possible reasons: recruitment or distension
Recruitment
at resting CO not all capillaries are perfused, as mean pressure ↑ closed capillaries are opened
Distension
as perfusion pressure ↑
cause distension ↑
radius ↓ resistance
Alveolar venrilation brings
O2 into lungs and removes CO2 from it
Pulmonary perfusion brings
CO2 into lungs and takes O2 out of lungs
PO2 and PCO2 are determined by
The relationships b/w alveolar ventilation (V) and perfusion (Q)
Amts in ventilation and perfusion
Ventilation: ~4 L/min
Perfusion: ~5 L/min
Q/V ratio
Ratio is 0.8

If inc in ratio then inc alveolar PO2 and dec alveolar PCO2
If dec ratio: dec alveolar PO2 and inc alveolar PCO2
Ventilation-Perfusion Extremes
Two extremes – no blood flow or no ventilation. Form continuum between the two
Control Mechanisms for ventilation-perfusion
Hypoxic Pulmonary vasoconstriction – alveolar hypoxia or atelectasis vasoconstricts precapillary vessels to shunt blood to non-hypoxic alveoli, occurs locally, effect limited by level of smooth muscle in pulmonary vasculature
Upper Lung Region and Ventilation
Intrapleural press more negative
Greater transmural press gradient
Alveoli larger & less compliant
Less ventilation
Upper Lung Region and Perfusion
Lower intravascular pressures
Less recruitment
Distension
Higer resistance
Less blood flow
Lower Lung Region and Ventilation
Intrapleural press less neg
Smaller transmural press gradient
Alveoli smaller & more compliant
More ventilation
Lower Lung Region and Perfusion
Greater vascular press
More recruitment
Distension
Lower resistance
Greater blood flow
Take Home for Lung regions
Lower regions of lung receive better perfusion and ventilation that the upper regions of the lung
Fick's Law for Diffusion
The rate of diffusion of a gas through the alveolar-capillary barrier is described by Fick’s Law for diffusion
Vgas =
.
Oxygen Diffusion
mixed venous blood PO2 40 mmHg , alveolar PO2 is 100 mmHg. It takes about 0.25 seconds to equilibrate ~ 1/3 of time blood is in capillary
CO2 Diffusion
mixed venous blood PCO2 is 45 mmHg, alveolar PCO2 is 40, it equilibrates in 0.25 seconds.