Respiratory phys part 2 and 3 Flashcards
What are the 4 lung volumes?
- tidal volume (amt of air inhaled or exhaled with each breath at rest)
- inspiratory reserve volume (inspiration above normal tidal volume)
- expiratory reserve volume (exhale beyond normal tidal volume, active expiration)
- residual volume (can’t measure with PFT, what is left over, necessary to keep lung inflated)
What are the 4 lung capacities?
(sum of 2 or more lung volumes)
- inspiratory capacity
- functional residual capacity
- vital capacity
- total lung capacity
What is the inspiratory capacity?
- TV+ IRV
- how much total can you inhale
What is functional residual capacity? (FRC)
- expiratory reserve volume + residual volume
What is the vital capacity (VC)?
- TV+ IRV+ ERV (total amt except RV)
What is TLC?
total lung capacity, sum of all lung volumes
TV+IRV+ERV+RV
What is a spirometer? Why is spirometry important?
- spirometer is an instrument used to measure respiratory volumes and capacities
- spirometry can distinguish between obstructive pulmonary disease - increased airway resistance (bronchitis)
and restrictive disorders - rduction in TLC due to structural or functional lung changes (fibrosis or TB)
What values can you obtain from spirometry?
- FVC: gas forcibly expelled after taking a deep breath
- FEV: amt of gas expelled during specific time intervals of FVC (FEV1= amt expelled in 1 second)
- peak expiratory flow rate
- flow volume loop
When would you see an increase in TLC, FRC, and RV?
- as a result of obstructive disease (can’t breathe out as easily)
When would you see a reduction in VC, TLC, FRC, and RV?
- result from restrictive disease
- smaller volumes, problems opening up airway
Why are PFTs ordered?
- to distinguish b/t obstructive and restrictive pulmonary disease
- useful for following course of disease
What is dead space?
alveolar dead space?
inspired air that never contributes to gas exchange
anatomical dead space: volume of the conducting zone conduits (150 ml)
- alveolar dead space: alveoli that cease to act in gas exchange due to collapse or obstruction
- total dead space: sum of above nonuseful volumes
What is alveolar ventilation rate? (AVR)
flow of gases into and out of alveoli during a particular time
AVR= breaths/minx (TV-dead space)
- this is the amount of air that will get into alveoli in one minute
- dead space is normally constant
- rapid, shallow breathing decreases AVR
What is MVR? AVR?
MVR= RRx TV
AVR= RR (TV-ds)
What is external and internal respiration?
external: lungs
internal: body tissues
What is Dalton’s law of partial pressures?
- total pressure exerted by a mix of gases is the sum of the pressures exerted by each gas
- the partial pressure of each gas is directly proportional to its percentage in the mix
What is Henry’s law?
gas will dissolve in a liquid in proportion to its partial pressure
- the amount of gas that will dissolve in a liquid also depends on it’s solubility and temp of liquid
- CO2 is 20x more soluble in water than O2
- very little N2 dissolves in water
- direction and movement of a gas are determined by its partial pressure: when pCO2 is higher in pulmonary capillaries than lungs CO2 will move into the lungs
- bigger the pressure gradient the faster the rate of exchange is
Why do alveoli contain more CO2 and water vapor than the atm?
due to:
- gas exchange in the lungs
- humidification of air
- mixing of alveolar gas that occurs with each breath
What is the partial pressure gradient for O2 in the lungs?
- it is steep, venous blood PO2 = 40 mm Hg
- alveolar PO2 = 104 mm Hg
- O2 partial pressures reach equil. of 104 in 0.25 seconds, about 1/3 the time of RBC is in a pulmonary capillary
What is partial pressure gradient for CO2 in the lungs?
- less steep
- venous blood PCO2 = 45 mm Hg
alveolar PCO2 = 40 mm Hg - CO2 is 20x more soluble in plasma than oxygen
- CO2 diffuses in equal amounts with oxygen
What is ventilation?
- amount of gas reaching alveoli
What is perfusion?
- blood flow reaching alveoli
What is ventilation-perfusion coupling?
- ventilation and perfusion must be matched (coupled, working together) for efficient gas exchange
What effect do changes in the PO2 in the alveoli have on diameters of the arterioles?
- where alveolar O2 is low, arterioles constrict in an attempt to redirect blood to areas where PO2 is higher
- where alveolar O2 is high, arterioles dilate to increase blood flow into the area to pick up the O2
What effect do changes in the PCO2 in the alveoli have on the diameters of the bronchioles?
- where alveolar CO2 is high, bronchioles dilate, this allows CO2 to be eliminated
- where alveolar CO2 is low, the bronchioles constrict
How thick are the respiratory membranes?
- 0.5 to 1 micrometer thick
- have large surface area (40x that of one’s skin)
- thicken if lungs become waterlogged and edematous and gas exchange becomes inadequate (pulmonary edema)
- reduction in surface area with emphysema, when walls of adjacent alveoli break down
What happens during internal respiration?
- capillary gas exchange in the body tissues
- partial pressures and diffusion gradients are reversed compared to external respiration
- PO2 in tissue is always lower than in systemic arterial blood
- PO2 of venous blood is 40 mm Hg and PCO2 is 45 mm Hg
2 ways that O2 is transported in the blood?
- 1.5% dissolved in plasma
- 98.5% loosely bound to each Fe of Hb in RBCs (4 O2/Hb)
What is oxyhemoglobin?
- O2 is attached
- reduced hemoglobin is Hb that has released O2
How is loading and unloading of O2 facilitated?
- by change in shape of Hb
- As O2 binds, Hb affinity for O2 increases
- in reverse, as O2 is released Hb affinity for O2 decreases
- Fully 100% saturated if all 4 heme groups carry O2
- partially saturated when 1 to 3 hemes carry O2
How is the rate of loading and unloading of O2 regulated?
- PO2
- temp
- blood pH
- PCO2
- concentration of BPG (rises when O2 uptake in lungs is compromised - altitude and obstructive lung disease)
Where is the highest % of saturated hemoglobin?
- in the arterial blood
- PO2 = 100 mm Hg
- Hb is 98% saturated
Why is Hb saturation lower in the venous blood?
- because of O2 uptake by the tissues
- PO2= 40 mm Hg
- Hb is 75% saturated
at what PO2 is hemoglobin almost completely saturated?
- when is O2 loading and delivery to tissues most adequate?
- at a PO2 of 70 mm Hg
- further increases in PO2 produce only small increases in O2 binding
- O2 loading and delivery to tissues is adequate when PO2 is below normal levels (offload more efficient - exercising tissues)
What % of bound O2 is unloaded during one systemic circulation?
- only 20-25% of bound O2 is unloaded
- if O2 levels in tissues drop: more O2 dissociates from Hb and is used by cells
- respiratory rate or cardiac output need not increase
What other factors other than PO2 influence Hb saturation?
- increases in temp, H+ (decreased pH), PCO2, and BPG
- modify the structure of Hb and decrease its affinity for O2
- occur in systemic capillaries
- enhance O2 unloading
- shift the O2 hb dissociation curve to the right (fever, metabolic rate increases- need increased O2)
- decreases in these factors shift the curve to the left (hypothermia)
What is BPG?
- 2,3-biphosphoglycerate
- produced by RBCs as they break down glucose through glyocolysis
- binds reversibly to Hb
- increases when O2 levels are critically low: decreases affinity of O2 for Hb allowing the O2 to be released (unbound) so that it can go to tissues where needed - ex: at high altitudes
How does the affinity for oxygen to Hb change as cells metabolize glucose?
- cellular respiration: cells metabolize glucose, use O2 and release CO2 so PCO2 and H+ increase in concentration in capillary blood - leads to decrease in pH
declining pH weakens the Hb-O2 bond (bohr effect) so that O2 is unloaded here (in tissues where it is most needed) - Heat production increases (by prod of metabolism): increasing temp directly and indirectly decreases Hb affinity for O2
What occurs during Hypoxia?
- inadequate O2 delivery to tissues
due to variety of causes: - too few RBCs (anemia) - abnormal or not enough Hb
- blocked circulation (pump failure or emboli)
- metabolic poisons (cyanide): changes binding of O2 to hemoglobin so O2 can still bind but can’t dissociate
- pulm disease (abnormal ventilation)
- CO (takes up O2 binding sites on Hb)
What are the 3 ways that CO2 is transported in the blood?
- dissolved in plasma (7-10%)
- bound to Hb (20%): binds to diff site than O2
- transported as bicarb ions in plasma (70%)
What does CO2 form when combined with water?
where does this occur most of the time?
- forms carbonic acid which quickly dissociates
- most of this occurs in RBCs
How does the transport of CO2 occur in systemic capillaries?
- HCO3 (bicarb) quickly diffuses from RBCs into the plasma
- then the chloride shift occurs: outrush of HCO3 from RBCs is balanced as Cl- moves in from the plasma
How does the transport and exchange of CO2 occur in the pulmonary capillaries?
- HCO3 moves into RBCs and binds with H+ to form H2CO3 (carbonic acid)
- H2CO3 is split by carbonic anhydrase into CO2 and water and CO2 then diffuses into the alveoli
What is the Haldane effect?
- the amount of CO2 transported is affected by the PO2
- the lower the PO2 and Hb saturation with O2, the more CO2 can be carried in the blood
- at the tissues, as more CO2 enters the blood: the more O2 dissociates from Hb (Bohr) and as Hb)2 releases O2, it more readily forms bonds with CO2 to form carbaminohemoglobin
What influence does CO2 have on blood pH?
- HCO3 in plasma is alkaline reserve of carbonic acid-bicarb buffer system
- if H+ concentration in blood rises, excess H+ is removed by combining with HCO3
- if H+ begins to drop, H2CO3 dissociates releasing H+
- changes in resp. rate can also alter blood pH - slow shallow breathing allows Co2 to accum. in blood causing the pH to drop
- changes in ventilation can be used to adjust pH when it is disturbed by metabolic factors
How do H+ ions and bicarb work to regulate blood pH?
- if H+ concentration in blood rises, then excess H+ is removed by combining with HCO3 to form carbonic acid and blood pH lowers (more acidic)
- if H+ concentration goes too low then carbonic acid dissociates and becomes HCO3 and pH increases (more alkalotic) ??
What parts of the brain is involved in neural control of respiration?
- involves neurons in the reticular formation of the medulla and the pons
- medulla: ventral respiratory group (VRG)
dorsal respiratory group - pons: pontine respiratory group
What factors influence respiration?
- neural mechanisms: medullary respiratory centers
pontine respiratory centers - chemical factors: arterial pH, PO2, and PCO2
- lung reflexes
- emotions (anxiety and pain)
Function of the DRG? Where is it located?
- near root of CN IX
- integrates input from peripheral stretch and chemoreceptors
Function of the VRG?
- rhythm generating and integrative center
- sets eupnea (12-15 breaths/min)
- inspiratory neurons excite the inspiratory muscles via the phrenic and intercostal nerves
- expiratory neurons inhibit the inspiratory neurons
Function of the pontine respiratory centers?
- influence and modify activity of VRG
- smooth out transition b/t inspiration and expiration and vice versa
Hypothesis of genesis of respiratory rhythm?
- not well understood
- most widely accepted that: reciprocal inhibition of 2 sets of interconnected neuronal networks in medulla sets the rhythm
How are depth and rate of breathing determined?
- depth is determined by how actively the respiratory center stimulates the respiratory muscles
- rate is determined by how long the inspiratory center is active
- both are modified in response to changing body demands
Chemical factors influence of PO2?
- peripheral chemoreceptors in the aortic and carotid bodies are O2 sensors: when excited they cause respiratory centers to increase ventilation
- substantial drops in arterial PO2 (to 60 mm Hg) must occur in order to stimulate increased ventilation
Chemical influence of arterial pH?
- can modify RR and rhythm even if CO2 and O2 levels are normal
- decreased pH may reflect:
CO2 retention, accum. of lactic acid, or excess ketone bodies in patients with DM - resp. system controls will attempt to raise the pH by increasing RR and depth
When does arterial PO2 become a major stimulus for respiration and via what?
- when it falls below 60 mm Hg, via the peripheral chemoreceptors
How do changes in arterial pH resulting from CO2 retention or metabolic factors act on respiration?
- indirectly through the peripheral chemoreceptors
What is the most powerful respiratory stimulant?
- rising CO2 levels
- normally blood PO2 affects breathing only indirectly by influencing peripheral chemoreceptor sensitivity to changes in PCO2
What is the influence of higher brain centers on respiration?
- hypothalamic controls act through the limbic system to modify rate and depth of respiration (emotional response)
- a rise in body temp increases RR
- cortical controls are direct signals from the cerebral motor cortex that bypass medullary controls: voluntary breath holding
What are the pulmonary irritant reflexes?
- receptors in the bronchioles respond to irritants
- promote reflexive constriction of air passages
- receptors in the larger airways mediate the cough and sneeze reflexes
What is the inflation reflex?
- Hering-Breuer Reflex: stretch receptors in the pleurae and airways are stimulated by lung inflation, inhibitory signals to the medullary respiratory centers end inhalation and allow expiration to occur
- acts more as a protective response than a normal regulatory mechanism
How do respirations adjust during exercise?
- adjustments are geared to both the intensity and duration of exercise
- hyperpnea: increase in ventilation (10-20 fold) in response to metabolic needs
- PCO2, PO2, and pH remain suprisingly constant during exercise
What 3 neural factors cause an increase in ventilation as exercise begins?
- phsycological stimuli: anticipation of exercise
- simultaneous cortical motor activation of skeletal muscles and respiratory centers
- excitatory impulses reaching respiratory centers from proprioceptors in moving muscles, tendons and joints
Why does ventilation decline suddenly when exercise ends?
- because the three neural factors shut off
What happens when you travel to altitudes above 8000 feet in a short time?
- may produce sxs of acute mountain sickness (AMS)
- HA, SOB,nausea, and dizziness
- in sever cases, lethal cerebral and pulmonary edema
What acclimatization respiratory adjustments are made when there is an increase in altitude?
- chemoceptors become more responsive to PCO2 when PO2 declines
- substantial decline in PO2 directly stimulates peripheral chemoreceptors
- the result is minute ventilation increases and stabilizes in a few days to 2-3 L/min higher than at sea level
What hematopoietic adjustments are made for the acclimatization to high altitude?
- decline in blood O2 stimulates the kidneys to accelerate production of EPO
- RBC numbers increase slowly to provide long-term compensation
- increased BPG
