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What would be the main anatomical features of a respiratory system?
- moist membrane
- opened pathway- trachea so gas can come in whenever it wants
- lots of surface area for gas exchange
- very thin membrane for diffusion
- elastic response- to both empty & fill the lungs
- highly vasculated- large amounts of capillaries
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Alveoli structure
- walls are made of simple squamous epithelial cells
- macrophages clean up particles that enter lungs
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Great alveoli cells
surfactant
- make surfactant
- -surfactant decreases natural surface tension in a water film
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"basket of capillaries"
- the capillary cells are "fused" to alveoli walls by an elastic basement membrane
- entire thickness is 0.5 microns
- BP is low so that osmotic pressure wins
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viseral pleura
outter tissue of the lungs, very thin membrane
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parietal pleura
lining under the rib cage, gives good surface tension
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pleural cavity
- really not meant to be a "space"
- -pleural cavity does have less pressure than in lungs
- -surface tension b/w 2 tissue layers: "pulls" on lungs when ribs are raised
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Pulmonary ventilation: inhalation
is active; need to create an internal pressure that is less than atmospheric pressure
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Pulmonary ventilation: exhalation
at rest is passive
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Boyle's Law
if you increase volume of a contained area you decrease pressure of gases w/in that area (inversely proportional)
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Charles's Law
gas volume will expand as temp. rises (directly proportional)
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Dalton's Law
- In a mixture of gases, each gas component exerts its own pressure
- -partial pressures: oxygen and carbon dioxide
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Pressures involved:
atmospheric
intrapulmonary pressure
intrapleural pressure
- atmospheric= 760 mm Hg
- intrapulmonary pressure= inside expanded lungs: 757
- intrapleural pressure= between ribs & visceral pleura 756-754
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Negative internal pressure
- pressure by raising ribs (intercostal muscles) and lowering diaphragm
- - as ribs move, they pull on lungs and aid in expansion due to surface tension b/w tissue
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Transpulmonary gradients
differences in pressures allow air flow into lungs
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Compliance
- ease of inhalation; little resistance to lung expansion
- Need: lungs easily expanded, muscles easily working ribs. alveoli easily open
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Factors that affect compliance
- elastic tissue in lungs
- residual air volume
- cartilage of ribs to be flexible
- surfactant to decrease surface tension b/w alveoli
- surface tension b/w viseral pleura and rib covering
- for exhalation: ease of recoil and fast relaxation of muscles
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pneumothorax
- increased pressure in pleural cavity
- -may lead to atelectasis: collapsed lung
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Partial Pressure of gases
HAVE TO READ NOTES!!!
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Ventilation
amount of air entering specific parts of lungs
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Perfusion
amount of blood entering the capillaries of the same part of the lungs
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What controls Hgb's affinity for oxygen?
- PO2 levels: higher pO2 means greater afinity
- -as the first O2 adds, this increases the affinity for more to add
- pH: increased acidity decreases affinity -H+ ions ling ot the Hgb; discourage affinity of O2-most significant in tissues where there is low pO2
Temp: increased in temp decreases affinity - -metabolically active tissues generate heat and need more O2
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Role of the 'waste' CO2
- very soluble in water
- -most will form carbonic acid
- -small percent stays as CO2 in the blood
- -small percent is carried around by the protein regions of Hgb
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Carbonic buffer system
HAVE TO READ NOTES!!!
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Details of gas exchange w/in the RBC's
- Shifting of H+ effects affinity of oxygen for Hgb
- -H+ shifts due to action of carbonic buffer system
- -H+ influences Hgb's affintiy for oxygen
- -Note systemic gas exchange details
- -Note alveolar gas exchange details
- Shifting of Cl ions encourages the buffer system in the tissue to shift to the R and stay there
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Hypercapnia
- leads to acidosis
- EX: reduced breathing rate due to coma
- CO2 levels and the buffer system go up and shift to the right
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Hypocapnia
- alkalosis
- EX: hyperventilation
- CO2 levels and the buffer system go down and shift left
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Regulation of breathing
- involuntary act over which you have voluntary control
- -chemoreceptors- in aorta & carotids closerly monitor blood pH
- -medulla oblongata- VRG & DRG
- - Pons- PRG
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Ventral respiratory group (VRG)
- has the inspiratory neurons
- -controls rhythm of breathing
- -at rest pace in about 12 breaths/min
- -inhalation take about 2 seconds
- -innervation from this region goes to diaphragm & external intercostals
- -absence of signal is expiration which takes about 3 seconds
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Dorsal Respiratory group
- used for heavy group
- ex: forced exhalation: active event
- can constrict the intercostals and abdominal muscles to force air out
- integrates messages coming from various areas inside and outside CNS
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Pneumotaxic area
- controls neurons in VRG
- needed to limit length and degree of inhalation
- impulses from VRG can be set at every 1/2 sec. (panting) to every 7 sec (prolonged inhalation)
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Other input to control centers that regulate breathing
- CC has some voluntary control; you can decide to alter breathing rate or hold your breath
- Chemoreptors for pH, also CO2 and oxygen levels
- stretch receptors in thoracic cavity send signals if you try to breath in too much! cant over inflate lungs
- changes in blood pressure and heart rate also have input
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COPD
- Chronic obstructive pulmonary disease
- Really 2 conditions combined: chronic bronchitis and emphysema
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bronchitis
caused by: allergies & asthma, smoking damage, repeated infections, pollution
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emphysema
- pulmonary fibrosis
- loss of alveoli; replace w/ fibrous connective tissue
- extreme increase in residual air volume
- lungs can not recoil enough to get old air out
- barrel chest results as patient struggles to expel air
- causes: smoking, genetic factors
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Lung cancer
- prolonged irritation from smoke means constantly replacing cells that line tubes
- increased rate of mitosis: increased rish of mutation; smoke is known carcinogen
- loss of cells impairs ability to clear lungs; smokers cugh and emphysema result
- mucous membrane of the large bronchial tubes are the most freguent sources of cancer cells
- spreads rapidly; poor prognosis
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infant respiratory distress syndrome
- premature infants have not produced surfactant
- -lungs close up after an exhale and infant can't re-inflate lungs
- treatment: man- made surfactant and high oxygen levels
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Cystic fibrosis
- msot common lethal genetic disease of Caucasians
- Two problems:
- 1.mucous produced in bronchial tubes is too thick
- -genetic flaw in ion transport
- -affects amount of fluid being put into mucous
- 2. Pancreas digestive enzymes don't reach the small intestine due to block duct
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