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151 Cards in this Set
- Front
- Back
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Completely removed in respiration
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PGE1
PGE2 F2 alpha Leukotrienes |
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Not effected by respiration
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PGA1
PGA2 PGI2 Epi Isoproterenol Dopamine ANG II |
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85%-90% removed in respiration
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5HT
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30% removed in respiration
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Norepinephrine
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80% removed in respiration
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Bradykinin
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70% converted in respiration
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70% of ANG I converted to ANG II
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40%-50% removed in respiration
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ATP and AMP
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Removed in plasma in respiration
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Acetylcholine
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Functions of Respiration
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gas exchange
acid-base balance (carbonic anhydrase) phonation (speech - air over vocal cords) control temp/humidity pulmonary defence mechanisms pulmonary metabolism |
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Pulmonary Defense Mechanisms
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ciliated epi
mucociliary elevator mucus cough reflex turbulent precipitation |
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Speed of Laminar Flow
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Fastest in the middle
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Volume and pressure change during contraction
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Increase volume in thoracic cavity
Decrease pressure in lung |
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If negative pressure inside and positive pressure outside, where will air flow?
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It will flow in
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Number of generations in bronchial tree
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23
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2 zones in bronchial tree
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Conducting zone
Transitional/Respiratory Zones |
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Conducting Zone
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150mL air
No gas exchange Generations 1-16 Trachea - bronchi - bronchioles - terminal bronchioles |
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Diameter, Length, Number, area in conducting zone
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Diameter: Decreases
Length: Decreases Number: Increases Area: Decreases from trachea to bronchioles. Increases from bronchioles to terminal bronchioles |
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Transitional/Respiratory Zone (AKA Acini)
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350mL air
gas exchange Generations 17-23 Respiratory bronchioles to alveolar ducts to alveolar sacs |
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Diameter, Length, Number, and area in Acini
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Diameter: Decreases
Length: Decreases Number: Increases Area: Increases |
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Number of alveoli in adults
Surface area for gas exchange |
300-480 million - avg is 300
50-100m^2 for gas exchange |
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Capillaries in bronchial tree
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280 billion capillaries cover the alveoli
500-1000 cap/alveolus |
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Distance of terminal bronchioles to most distant alveolus
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5mm
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Primary Bronchi
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generation 1, enter lung at Hilus
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Segmental Bronchi
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generation 3
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Bronchioles
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generation 4-16
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Terminal Bronchioles
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generation 16
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Conduction Airways
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nose to terminal bronchioles – anatomical dead space
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Respiratory Bronchioles
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have alveoli budding off
generations 17-19 transition |
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Alveolar Ducts
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completely lined with alveoli
generations 20-22 |
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Alveolar Sacs
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groups of alveoli
generation 23 |
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Barriers to get blood across
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Alveolar Epithelial Cells
Interstitial Space Capillary Endothelial cells Erythrocyte - combine w/ hemoglobin |
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Time for gas exchange in capillaries
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Normal breathing: 3/4 s
Fast breathing: 1/4 s |
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What is very important in bronchiolar structure?
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Tone
EX: asthma is over sensitive smooth muscle response |
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Receptors for asthma
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B2: albuterol on bronchial smooth muscle and relax it
Muscarinic: (ACH) receptors that contract |
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Structure of tissue on bronchus
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mucous blanket
cilia goblet cells epi smooth muscle mucous gland submucosal ct cartliage |
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Structure of tissue in bronchiole
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cilia
goblet cells epi smooth muscle sumucosal ct |
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Structure of tissue in alveolus
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.
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Type 1 Pneumocyte
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thin squamous cells flattened nucleus
95 % of surface area of alveoli |
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Type 2 Pneumocyte
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cuboidal shaped cells located at corners of alveoli
5% of surface area, synthesize surfactant and precursor of type I cells |
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Alveoli
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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 |
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Blood-Gas Barriers
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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 |
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Tidal Volume
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volume expired or inhaled with each normal breath ~ 500 mls
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Inspiratory Reserve Volume
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volume that can be inspired after a normal tidal
volume ~ 3100 mls |
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Expiratory Reserve Volume
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volume forcefully exhaled after a normal tidal
volume ~ 1200 mls |
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Residual Volume
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volume remaining in the lungs after forceful exhalation
~ 1200 mls |
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Inspiratory capacity
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Inspired reserve volume plus tidal volume
~ 3600 mls |
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Vital capacity
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Maximum amount of air that can be expired following maximum filling of lungs
~ 4800 mls |
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Total lung capacity
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maximum volume of lung expansion
~ 6000 mls |
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Functional Residual Capacity (FRC)
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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 |
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Minute respiratory volume
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tidal volume X respiratory rate
~ 500 mls X 12/min = 6000 mls |
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minute alveolar ventilation
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new air reaching gas exchange area of lungs ~ 500– 150 mls (anatomical dead space X respiratory rate = 350 X 12 = 4200 mls
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Forced expiratory volume (FEV)
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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
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Negative Pressure Breathing
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normal due to alveolar pressure
< atmospheric pressure |
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Positive Pressure Breathing
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done by machines on patients that can’t ventilate properly atmospheric > alveolar pressure
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Air Flow moves
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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
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Poiseuille's Law
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F= ΔP/R
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R equals
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R = η x L x 8/π x r^4
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Flow (V) equals
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V = ΔP x π x r^4/η x L x 8
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Boyle's Law
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Pressure and volume are inversely related
Applies to diaphram contraction |
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pneumothorax
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hole in lung
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Alveolar Pressure Equals
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Alveolar pressure = pressure inside of alveolar space, at rest equal to atmospheric pressure (760 mm Hg or 0 cm H20)
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When does air flow out of the lungs?
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Air flows out of lungs when alveolar pressure is sufficiently greater than atmospheric pressure to overcome the resistance of the airways
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When does air flow into lungs?
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Air flows into lungs when alveolar pressure less that atmospheric and can overcome resistance
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Why do muscle of inspiration contract?
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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.
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What is intrapleural pressure equal to?
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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.
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Why is intrapleural pressure negative?
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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
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Transmural Pressure Gradient (TMP) equals
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TMP = alveolar pressure - intrapleural pressure
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Principal of TMP
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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
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How is the pressure gradient across the outermost alveoli transmitted?
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The pressure gradient across the outermost alveoli is transmitted mechanically through the lung via the alveolar septa
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Diaphragm
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dome shaped muscle separates thorax from abdominal cavity, innervated by phrenic nerves which leave spinal cord at 3rd -5th cervical segments.
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Movement of diaphragm during breathing
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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
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Intercostal muscles during inspiration
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External Intercostal
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Intercostal muscles during expiration
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Internal Intercostal
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External Intercostals
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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. |
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Dyspnea
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feeling of breathing difficulty may be caused by fatigue of inspiratory muscles
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ACH and diaphragm
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Nerve fibers activated by release of ACH on nicotinc receptors. Diaph contracts
Ca2+ - actin - myosin - tropomysin - back to SR to relax. |
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Expiration is what during normal quiet breathing?
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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
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Which muscles are involved in active respiration?
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include muscles of abdominal wall:
rectus abdominis external and internal oblique transverse abdominis internal intercostals |
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Transpulmonary Pressure
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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 |
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Compliance Equals
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Change vol/Change press
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Compliance represents
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the ease with which something can be stretched or distorted
It is the inverse of elasticity |
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Elasticity
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Tendency to resist stretch or distension
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Compliance and Isolated Lungs
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where changes in lung volume were graphed against changes in pressure
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Hysteresis
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difference in curves: caused by surfactant, and recruitment of alveoli
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Chest Muscles and Compliance
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Chest muscles also show compliance
1/total compliance = 1/lung + 1/chest wall |
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Lung Compliance Circuit
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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) |
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Fibrosis
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due to tissue damage makes lungs less compliant or stiffer, increase elastic recoil. Collapsed alveoli (atelectasis) also make the lung less compliant
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Emphysema
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due to loss of septal walls that oppose lung expansion make the lungs more compliant
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Surface Tension Forces
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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. |
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LaPlace's Law
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P (dyn/cm) = 2 x T (dyn/cm)/r (cm)
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T equals
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P x r/2
T= tension on outside P= press grad in h2o drop r= radius of sphere inside h2o drop |
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Droplet size is determined by?
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Droplet size is determined by point at which pressure of fluid inside droplet equals tension of droplet to collapse
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How are 2 alveoli of diff size connected?
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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
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If surface tension is controlled...
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the smaller alveoli will not collapse
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Surfactant is made of
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85-90% lipids and 10-15% proteins, 75% diplamitoyl phosphatidylcholine, 4 surfactant proteins SP-a, SP-B, SP-C and SP-D
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Surfactant Production
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Continuously produced by type II pneumocytes and taken back into type II cells to be degraded into other phospholipids
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Functions of surfactant
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stabilize alveoli, lower surface tension of smaller alveoli, increases compliance of lungs, decreases elastic recoil of lungs and decreases work of inspiration
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Clinical Consequences of surfactant
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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.
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Treatment of mother
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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.
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What can decrease surfactant?
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Hypoxia or hypoxemia may decrease surfactant or increase breakdown and adult respiratory distress syndrome or Shock-lung seen after trauma or surgery)
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Alveolar Interdependence
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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.
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How does alveolus respond to collapse?
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If an alveolus tries to collapse it puts pressure on surrounding alveoli that will help keep it open
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Surface Tension & the Interior and Exterior elastic Recoil
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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)
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What if the integrity of the lung-chest wall system is damage?
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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.
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Resistance and Change in pressure
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Change in P = flow x resistance
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Resistance in circuit
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In Parallel: are added as reciprocals
In Series: Are additive |
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Pooseuille's Law Governs
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movement of fluid through tubes
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Change is Pressure is directly proportional to
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Airflow (V) x Resistance (R)
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F =
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F = Change P/R
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R =
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Flow (V) =
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When does turbulent flow occur?
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Reynolds number above 2000
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Re =
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.
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Airway Resistance
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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)
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What constricts bronchiolar smooth muscle?
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-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) |
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What relaxes bronchiolar smooth muscle?
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-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 |
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Forced expiration and intrapleural pressure
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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
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How long does it take for FEV expiration?
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In normal ind: 80% of FEV in 1st second.
Significantly longer if airway obstruction or collapse. |
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Airflow Volume Curves
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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, |
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Where do lungs receive blood from?
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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 |
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Pulmonary Blood Flow At Rest
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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.
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RBC's and pulmonary blood flow
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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.
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Pulmonary Capillaries and alveoli for gas exchange
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280 billion pulmonary capillaries supply 300 million alveoli so gas exchange area is 50-100 m2
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Blood flows from the bronchial artery to?
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The bronchiolar tree down to the level of the terminal bronchi receive blood flow from the bronchial artery
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Structures distal to the terminal bronchioles received oxygen from?
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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
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Pulmonary Veins carry?
Pulmonary Arteries carry? |
Pulmonary veins carry oxygenated blood
Pulmonary arteries carry low oxygen blood |
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Pulmonary Circulation Is
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Pulmonary circulation is a low pressure system and is much thinner walled and more distensible and compressible than systemic circulation
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Differences in Pulmonary Vessles
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-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 |
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Alveolar Pulmonary Perfusion
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As lung volume ↑, alveoli ↑ in volume stretch capillaries, ↑ length, ↓ diameter, increase resistance.
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Extra Alveolar Pulmonary Perfusion
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increased negative intrapleural pressure, stretches vessels to ↑ diameter, ↓ resistance
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Positive Pressure Breathing
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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) |
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During exercise when CO increases several fold, what happens to mean arterial pressure?
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CO may inc several fold w/o a corresponding inc in mean arterial pressure unlike systemic circulation.
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In isolated lung, as blood flow increases what happens to vasular resistance?
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Vascular resistance will decrease.
Inc blood flow w/o working as hard. 2 possible reasons: recruitment or distension |
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Recruitment
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at resting CO not all capillaries are perfused, as mean pressure ↑ closed capillaries are opened
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Distension
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as perfusion pressure ↑
cause distension ↑ radius ↓ resistance |
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Alveolar venrilation brings
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O2 into lungs and removes CO2 from it
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Pulmonary perfusion brings
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CO2 into lungs and takes O2 out of lungs
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PO2 and PCO2 are determined by
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The relationships b/w alveolar ventilation (V) and perfusion (Q)
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Amts in ventilation and perfusion
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Ventilation: ~4 L/min
Perfusion: ~5 L/min |
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Q/V ratio
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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 |
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Ventilation-Perfusion Extremes
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Two extremes – no blood flow or no ventilation. Form continuum between the two
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Control Mechanisms for ventilation-perfusion
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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
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Upper Lung Region and Ventilation
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Intrapleural press more negative
Greater transmural press gradient Alveoli larger & less compliant Less ventilation |
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Upper Lung Region and Perfusion
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Lower intravascular pressures
Less recruitment Distension Higer resistance Less blood flow |
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Lower Lung Region and Ventilation
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Intrapleural press less neg
Smaller transmural press gradient Alveoli smaller & more compliant More ventilation |
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Lower Lung Region and Perfusion
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Greater vascular press
More recruitment Distension Lower resistance Greater blood flow |
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Take Home for Lung regions
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Lower regions of lung receive better perfusion and ventilation that the upper regions of the lung
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Fick's Law for Diffusion
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The rate of diffusion of a gas through the alveolar-capillary barrier is described by Fick’s Law for diffusion
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Vgas =
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.
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Oxygen Diffusion
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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
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CO2 Diffusion
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mixed venous blood PCO2 is 45 mmHg, alveolar PCO2 is 40, it equilibrates in 0.25 seconds.
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