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Phys U4 - Resp

Physiology Unit 4 - Respiratory - Fofi

Respiratory system functions to supply body with oxygen, dispose of CO2
Respiration—four processes pulmonary ventilation, external ventilation, transport, internal respiration
Pulmonary ventilation moving air into and out of lungs
External respiration gas exchange b/t lungs and blood
Transport transport of O and CO2 b/t lungs and tissues
Internal respiration gas exchange b/t systems blood vessels and tissues
Respiratory system components conducting and respiratory zones, respiratory muscles
Conducting zone provides rigid conduits for air to reach sites of gas exchange; nose, nasal cavity, pharynx, trachea, primary bronchi, smaller bronchi; air passages undergo 23 orders of branching in the lungs, significantly increasing cross sectional area for flow
Respiratory zone site of gas exchange; consists of bronchioles, alveolar ducts, alveoli; approximately 300 million alveoli; account for most of the lung’s volume, provide tremendous surface area for gas exchange
Internal respiration exchange of gases between interstitial fluid and cells
External respiration exchange of gases between interstitial fluid and the external environment; steps include pulmonary ventilation, gas diffusion, transport of O and CO2
Pulmonary ventilation physical movement of air into and out of lungs; mechanical process that depends on volume changes in thoracic cavity; volume changes lead to pressure changes, which lead to flow of gases to equalize pressure. Gas moves from high pressure to low pressure
Boyle’s Law relationship b/t pressure and volume of gases; P1V1=P2V2; P=pressure of gas in cubic millimeters; V=volume of a gas in cubic mm; inversely proportional, so as pressure decreases, volume increases; as volume decreases, pressure increases
Diaphragm movement at rest diaphragm relaxed; as diaphragm contracts, thoracic volume increases; diaphragm relaxes, thoracic volume decreases
Pressure relationships in thoracic cavity respiratory pressure is always described relative to atmospheric pressure
Atmospheric pressure (pATM) pressure exerted by the air surrounding the body (760mmHg at sea level); negative respiratory pressure is less than pATM; positive respiratory pressure is greater than pATM
Intrapulmonary pressure pressure within the alveoli is ~760mmHg when even with pATM
Intrapleural pressure pressure within the pleural cavity which adheres lungs to thoracic cavity; ~756mmHg
What holds the thoracic wall and lungs together? the two forces of intrapulmonary and intrapleural pressure hold the thoracic wall and lungs in close apposition—stretching the lungs to fill the thoracic cavity
Intrapleural fluid cohesiveness polarity of water attracts wet surfaces
Transmural pressure gradient pATM (760mmHg) is greater than intrapleural pressure (756mmHg) so lungs expand; elastic recoil of chest wall tries to pull chest outward; elastic recoil of lung creates inward pull
Intrapulmonary & intrapleural pressure relationships intrapulmonary pressure and intrapleural pressure fluctuate w/ phases of breathing; intrapulmonary pressure always eventually equalizes itself w/ pATM; intrapleural pressure is always less than intrapulmonary pressure and pATM
Respiratory mechanics changes in intra-alveolar pressure produce flow of air in & out of lungs; if this pressure is < pATM, air enters; if > pATM, air exits; boyle’s law states—any constant temp, pressure exerted by a gas varies inversely w/ the volume
Inspiration diaphragm, external intercostals contract—rib cage rises; lungs stretched, intrapulmonary vol increases; intrapulmonary pressure drops below pATM (-1); air flows into lungs down pressure gradient, until intrapulmonary pressure = pATM
Expiration inspiratory muscles relax, rib cage descends; thoracic cavity vol decreases; lungs recoil, intrapulmonary vol decreases; intrapulmonary press. Rises > pATM +1; gases flow out of lungs down pressure gradient until intrapulmonary pressure is equalized
Respiratory cycle single cycle of inhalation and exhalation; amount of air moved in one cycle is tidal volume
Tidal volume (TV) amount of air moved in one respiratory cycle (single cycle of air inhalation and exhalation)
Physical factors influencing ventilation friction is the major nonelastic force of resistance to air flow; compliance, elastic recoil
Resistance and ventilation relationship b/t flow (F), pressure (P), and resistance (R) is Flow= ΔP /R; friction is the major non-elastic source of resistance
Compliance ability to stretch; ease with which lungs can be expanded due to change in transpulmonary pressure; determined by distensibility of lung tissue and surrounding thoracic cage and surface tension of alveoli; can be high or low
Restrictive lung diseases fibrotic lung diseases and inadequate surfactant production will produce low compliance.
Elastic recoil return to resting vol when stretching force released; connective tissue elasticity--lungs assume smallest possible size; surface tension of alveoli draws them to their smallest possible size; elastance—measure of how readily lungs rebound after stretching
Alveolar surface tension attraction of liquid molecules to one another at liquid-gas interface; thin layer b/t alveolar cells and air; always acting to reduce alveoli to smallest poss size; surfactant reduces to keep alveoli from collapsing
Surfactant detergent-like complex secreted by type II alveolar cells; reduces surface tension and helps keep the alveoli from collapsing
Airway resistance gas flow is inversely proportional to resistance with the greatest resistance being in the medium-sized bronchi; severely constricted or obstructed bronchioles—COPD
Emphysema destruction of alveoli reduces surface area for gas exchange
Fibrotic lung disease thickened alveolar membrane slows gas exchange; loss of lung compliance
Pulmonary edema fluid in interstitial space increases diffusion distance
Asthma increased airway restriction decreases airway ventilation
Lung capacity/volume lungs can be filled to over 5.5L on max inspiratory effort; emptied to 1L on max expiratory effort; normally operate at “half-full” 2-2.5L; on avg. 500ml moved in/out w/ each breath
Tidal volume (TV) air that moves in and out of lungs with each breath (~500ml)
Inspiratory reserve volume (IRV) air that can be inspired forcibly beyond the tital volume (2100-3200ml)
Expiratory reserve volume (ERV) air that can be evacuated from the lungs after a tidal expiration (1000-1200ml)
Residual volume (RV) air left in lungs after strenuous expiration
Inspiratory capacity (IC) total amount of aire that can be inspired after a tidal expiration (IRV + TV)
Functional residual capacity (FRC) amount of air remaining in lungs after tidal expiration (RV+ERV)
Vital capacity (VC) total amount of exchangeable air (TV+IRV+ERV)
Total lung capacity (TLC) sum of all lung volumes (~6000ml in males)
Anatomical dead space volume of conducting respiratory passages (150ml)
Alveolar dead space alveoli that cease to act in gas exchange due to collapse or obstruction
Total dead space sum of alveolar and anatomical dead spaces
Factors influencing movement of O and CO2 across respiratory membrane partial pressure gradients & gas solubilities; matching of alveolar ventilation and pulmonary blood perfusion; structural characteristics of respiratory membrane
Dalton’s law total pressure exerted by mixture of gases=sum of pressures exerted independently by each gas in mixt; partial pressure of ea gas directly proportional to its % in mix; PO2 air is 20.93% O2; total pressure of air is 760mmHg; PO2=.2093x760=159mmHg
Henry’s law when mixture of gases in contact w/ a liquid, each gas will dissolve in the liquid in proportion to its partial pressure; amount gas dissolved also depends on solubility; CO2 most soluble; O2 1/20th as soluble; nitrogen practically insoluble in plasma
Gas diffusion gases diffuse from high to low partial pressure between lung and blood/between blood and tissues
Respiratory membrane only .5-11 mm thick, allowing for efficient gas exchange; total surface area of about 60m2; air-blood barrier composed of alveolar and capillary walls; alveolar walls are single layer type I epithelial cells
Alveolar gas contain more CO2 & water vapor, while atmosphere is mostly nitrogen and oxygen; differences result from gas exchanges in lungs, humidification of air, mixing of alveolar gas w/ each breath
Partial pressure gradients PO2 of venous blood is 40mmHg; PO2 in alveoli is ~100mmHg; steep gradient allows PO2 gradients to rapidly reach equilibrium; blood can move quickly thru pulmonary capillary and still be adequately oxygenated
Internal respiration factors promoting gas exchange b/t systemic capillaries & tissue cells are same as in lungs—partial pressures & diffusion gradients reversed; PO2 in tissue always lower than in systemic arterial blood; PO2 venous blood draining tissues—40mmHg, PCO2 45mmHg
Ventilation-perfusion coupling ventilation—amt gas reaching alveoli; perfusion—blood flow reaching alveoli; must be tightly regulated for efficient gas exchange; chgs in PCO2 in alveoli causes chgs in diameters of pulmonary arterioles
Alveolar CO2 high/O2 low vasoconstriction
Alveolar CO2 low/O2 high vasodilation
O2 transport in blood 3 methods—dissolved in plasma; bound to Hb in blood—oxyhemoglobin (O2 bound to Hb) or deoxyhemoglobin (O2 not bound to Hb)
Saturated hemoglobin when all four hemes of the molecule are bound to oxygen
Partially saturated hemoglobin when one to three hemes are bound to oxygen
Rate that hemoglobin binds with oxygen regulated by PO2, temperature, blood pH, PCO2
Hemoglobin saturation curve Hb saturation plotted against PO2 produces oxygen-hemoglobin dissociation curve; at 100mmHg, Hb 98% saturation; saturation of Hb is why hyperventiliation has little effect on arterial O2 levels
Influence of PO2 on Hb saturation 98% saturated arterial blood—20ml O2/100ml blood (20%vol); only 20-25% of bound O2 unloaded during one systemic circulation; if O2 levels in tissues drop, more O2 dissociates from Hb, used by cells; respiratory rate/CO output need not increase
Factors influences Hb saturation temperature, H+, PCO2, and BPG alter Hb affinity for O2; increases of factors decreases Hb affinity for O2 and enhance O2 unloading from blood; these paramteres are high in tissue capillaries where O2 unloading is goal
Bohr effect H+ and CO2 modify the structure of Hb
CO2 transport in blood in three forms—dissolved in plasma, chemically bound to Hb as carbaminohemoglobin; bicarbonate ion in plasma
Transport and exchange of CO2 CO2 quickly diffuses into RBCs and combines with H20 to form carbonic acid H2CO3, which quickly dissociates into hydrogen ions and bicarbonate ions; CO2+H20«H2CO3«H+HCO3-
Carbonic acid-bicarbonate buffer system system resists blood pH changes; if H+ in blood increases, excess H+ is removed by combining w/ HCO3; if H+ decreases, carbonic acid dissociates, releasing H+
Chloride shift at tissues, bicarbonate quickly diffuses from RBCs into plasma; chloride ions move from plasma into RBCs to counterbalance out rush of negative bicarbonate ions
CO2 transport at lungs bicarbonate ions move into rBCs, bind w/ H+ ions, form carbonic acid; Carbonic acid split by carbonic anhydrase to release CO2 and H20; CO2 diffuses from blood into alveoli
Haldane effect removing O2 from Hb increases ability of Hb to pick up CO2 and CO2 generated H+ ; works in synch w/ bohr effect to facilitate O2 liberation, uptake of CO2 & H+
Control of respiration medullary respiratory centers
Dorsal respiratory group DRG inspiratory center; inspiratory neurons, thought to be set by basic rhythm “pacemaking”; excited inspiratory muscles and sets eupnea (12-15 breaths/min); cease firing during expiration
Ventral respiratory group inspiratory & expiratory neurons; remains inactive during quiet breathing; activity when demand is high; involved in forced inspiration and expiration
Pons respiratory centers/pontine respiratory group influence and modify activity of medullary centers to smooth out inspiration & expiration transitions; consists of pneumotaxic center, apneustic center
Pneumotaxic center part of pontine respiratory group; sends impulses to DRG to switch off inspiratory neurons, limiting duration of inspiration; dominates to allow expiration to occur normally
Apneustic center prevents inspiratory inhibition to provide increase inspiratory drive when needed
Depth & rate of breathing inspiratory depth—determined by how actively respiratory center stimulates respiratory muscles; rate of resp determined by how long inspiratory center is active; resp centers in pons/medulla sensitive to both excitatory & inhibitory stimuli
Input to respiratory centers cortical controls, hypothalamic controls, temperature, pulmonary irritants, inflation reflex
Cortical controls input to respiratory centers; direct signals from cerebral motor cortex that bypass medullary controls (ex. voluntary breath holding, taking a deep breath)
Hypothalamic controls input to respiratory centers; act through the limbic system to modify rate and depth of respiration; ex. breath holding that occurs in anger
Temperature and respiratory rate input to respiratory centers; rise in body temperature acts to increase respiratory rate
Pulmonary irritant reflexes input to respiratory centers; irritants promote reflexive constriction of air passages
Inflation reflex (Hering-Breuer) input to respiratory centers; stretch receptors in lungs are stimulated by lung inflation; upon inflation inhibitory signals sent to medullary inspiration center to end inhalation, allow expiration
PCO2 and breathing depth and rate PCO2 lvls monitored by brain stm chemoreceptors; blood CO2 diffuses into CSF & hydrated, H2CO3 dissociates, releases H+ ions; PCO2 increases, increases breathing depth/rate; CO2 rise is stimulus, control of breathing @ rest regulated by H ion brain conc.
Peripheral chemoreceptors regulate ventilation; located in carotid and aortic arteries; specialized glomus cells; sense changes in PO2, pH, PCO2
Hyperventilation increased depth and rate of breathing that quickly flushes CO2 from blood; occurs in response to hypercapnia (increased PCO2); though CO2 is original stimulus, control of breathing at rest is regulated by H+ ion concentration in brain
Hypoventilation slow, shallow breathing due to abnormally low PCO2 levels
Apnea may occur until PCO2 levels rise
Arterial pH + breathing changes can modify respiratory rate even if CO2 & O2 levels are normal; increased ventilation in response to falling pH mediated by peripheral chemoreceptors
Acidosis condition may reflect CO2 retention, accumulation of lactic acid, excess fatty acids in patients with diabetes mellitus
Low pH respiratory system controls will attempt to equilibrate by increasing respiratory rate and depth
High pH respiratory system will attempt to equilibrate by decreasing rate and depth of breathing
Created by: michellerogers



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