Ch. 23 - Respiratory System Flashcards
Respiration
gas exchange between O2 and CO2. Occurs between atmosphere and body cells and involves 4 processes (pulmonary ventilation, alveolar gas exchange, gas transport, and systemic gas exchange)
Respiratory system
provides means for gas exchange; consists of respiratory passageways in head, neck, trunk, and lungs.
4 processes of Respiration
Pulmonary ventilation: movement of gases between atmosphere and alveoli.
Alveolar gas exchange (external respiration): exchange of gases between alveoli and blood.
Gas Transport: transport of gases in blood between lungs and systemic cells.
Systemic gas exchange (internal respiration): exchange of respiratory gases between the blood and systemic cells.
4 processes of Respiration
Pulmonary ventilation: movement of gases between atmosphere and alveoli.
Alveolar gas exchange (external respiration): exchange of gases between alveoli and blood.
Gas Transport: transport of gases in blood between lungs and systemic cells.
Systemic gas exchange (internal respiration): exchange of respiratory gases between the blood and systemic cells.
8 steps of respiratory gas movement
- Air containing O2 is inhaled into alveoli during inspiration (pulmonary ventilation)
- O2 diffuses from alveoli into pulmonary capillaries (alveolar gas exchange)
- Blood from lungs transports o2 to systemic cells (gas transport)
- O2 diffuses from systemic capillaries into systemic cells (systemic gas exchange)
- CO2 diffuses from systemic cells into systemic capillaries. (systemic gas exchange)
- CO2 is transported in blood from systemic cells to lungs (gas transport)
- Co2 diffuses from pulmonary capillaries into alveoli (alveolar gas exchange)
- Air containing CO2 is exhaled from alveoli into atmosphere (pulmonary ventilation)
Pulmonary ventilation
process of moving air into and out of lungs. Amount of air moved between atmosphere and alveoli in 1 min; consists of two cyclic phases: inspiration (bringing air into lungs) and expiration (forces air out of lungs). Autonomic nuclei in brainstem regulate breathing activity. Skeletal muscles cause volume and pressure gradient changes and the air moves down its pressure gradient.
Quiet breathing (eupnea)
rhythmic breathing at rest
Forced breathing
vigorous breathing accompanies exercise
Muscles of quiet breathing
diaphragm: flattens when it contracts
External intercostals: elevate ribs
These muscles relax for expiration.
Muscles of forced inspiration
sternocleidomastoid, scalenes, pectoralis minor, and serratus posterior superior, contract for deep inspiration. internal intercostals, abdominal muscles, transversus thoracis, and serratus posterior inferior contract for hard expiration (coughing). These move the rib cage superiorly, laterally, and anteriorly. Erector spinae, located along length of vertebral column; contracts to help lift rib cage. Collectively termed accessory muscles of breathing when paired with the muscles of forced inspiration.
Vertical Thoracic volume change
result from diaphragm movement. Only small movements required for relaxed breathing.
lateral dimension thoracic changes
rib cage elevation widens and narrows. Changes due to all breathing muscles except diaphragm
anterior-posterior thoracic dimension changes
inferior part of sternum moves anteriorly in inspiration and changes due to all breathing muscles except diaphragm.
Boyles gas law
at a constant temp., pressure of a gas decreases as volume increases; inverse relationship.
P1V1 = P2V2
Pressure Gradient
exists when force per unit area is greater in one place than another. If the areas are interconnected, air will flow down pressure gradient. can be changed by altering volume of thoracic cavity. (small volume changes of quiet resp. only allow .5 L to enter)
Atmospheric pressure
total pressure that all gases exert in the environment; changes with altitude (lower pressure with high altitude). 1 atm = 760 mm Hg at sea level.
Alveolar volume
collective volume in alveoli. Includes intrapulmonary pressure (in alveoli) and intrapleural pressure (in pleural cavity).
Intrapulmonary pressure
pressure in alveoli. Is equal to atm at end of inspiration and expiration
Intrapleural pressure
Pressure in pleural cavity; fluctuates with breathing. Is lower than intrapulmonary pressure (keeps lungs inflated). About 4 mm Hg lower than intrapulmonary between breaths.
Quiet breathing: expiration
- Initially, intrapulmonary pressure = atmospheric pressure. Intrapleural pressure is about 6 mm Hg lower.
- Diaphragm and external intercostals relax decreasing thoracic volume. Pleural cavity vol. decreases, so intrapleural pressure increases. Elastic recoil pulls lungs inward, so alveolar vol. decreases and intrapulmonary pressure increases. Since intrapulmonary pressure is greater than atm, air flows out until these pressures are equal. About .5 L of air leaves the lung.
Quiet breathing: inspiration
- Intrapulmonary pressure and Atmospheric pressure are initially equal (760 mg Hg). Intrapleural pressure is 4 mm Hg lower.
- Diaphragm and external intercostals contract increasing thoracic volume. Diaphragm accounts for 2/3 of volume change and external intercostal accounts for 1/3. Lungs are pulled by pleurae, so lung vol. increases and intrapulmonary pressure decreases. Because intrapulmonary pressure is less than atm, air flows in until equal (typically .5 L)
Forced breathing
involves similar steps to quiet breathing and contraction of additional muscles.
Airflow
amount of air moving in and out of lungs with each breath. Dependent on Pressure Gradient between atm and intrapulmonary pressure and Resistance.
What nuclei coordinate breathing
Autonomic; specifically the respiratory center of the brainstem. This consists of the medullary respiratory center (containing ventral and dorsal respiratory groups) and the pontine respiratory center in the pons; also known as pneumotaxic center.
Brainstem neurons
influence respiratory muscles. VRG (ventral respiratory group) neurons synapse with lower motor neurons of skeletal muscles in spinal cord. Lower motor neuron axons project to respiratory muscles. Axons innervating diaphragm travel in phrenic nerves. Axons innervating intercostal travel in intercostal nerves.
Chemoreceptors
monitor changes in concentrations of H, PCO2 and PO2.
Central Chemoreceptors
in medulla and monitors pH of CSF. CSF pH changes are caused by changes in blood PCO2. CO2 diffuses from blood to CSF where carbonic anhydrase is and that builds carbonic acid from co2 and h20.
Peripheral chemoreceptors
are in aortic and carotid bodies. Stimulated by changes in H or respiratory gases in blood. Respond to H produced independently of CO2. Carotid chemoreceptors send signals to respiratory center via glossopharyngeal nerve and aortic chemoreceptors send signals to resp. center via vagus nerve.
Irritant receptors
receptor that influences respiration; includes sneeze and cough reflex. in air passageways and stimulated by particulate matter. Causes an exaggerated intake of breath followed by closure of larynx and contraction of abdominal muscles for explosive blast of exhaled air.
Baroreceptors
in pleurae and bronchioles that influence respiration in response to stretch. Sends signals to respiratory center when overstretched to initiate inhalation reflex (to shut off inhalation)
Proprioceptors
in muscles and joints and influence respiration based on body movement. Signal respiratory center to increase breathing depth
Physiology of quiet breathing
Inspiration begins when VRG inspiratory neurons fire spontaneously. Signals are sent from VRG to nerves exciting skeletal muscles for about 2 sec causing diaphragm and ex. intercostals to contract and air flow in. quiet expiration occurs when VRG is inhibited. Signals from inspiratory neurons are relayed to VRG expiratory neurons and expiratory neurons send inhibitory signals back so that no signals are sent to inspiratory muscles for about 3 secs.
Normal respiration rate
12-15 breaths per min.
Pontine respiratory center
facilitates smooth transitions between inspiration and expiration by sending signals to medullary resp. center. Damage to pons causes erratic breathing.
how do chemoreceptors alter breathing rate and depth?
by sending signals to DRG (dorsal resp. group) which are relayed to VRG. VRG changes rhythm and force of breathing by altering amount of time in inspiration and expiration and stimulation of muscles.
What causes an increase in ventilation?
- central chemoreceptors detecting an increase in H concentration of CSF
- Peripheral chemoreceptors detecting increase in blood H or PCO2
Increased ventilation will expel more Co2 returning conditions to normal. Decrease ventilation will occur if opposites happen.
How does blood PCO2 influence breathing?
It is the most important stimulus affecting breathing; raising it by 5 mm Hg doubles breathing rate.Co2 fluctuations influence sensitive central chemoreceptors and it combines with water in CSF to form carbonic acid. CSF lacks buffers so its pH change triggers reflexes. Blood po2 is not as sensitive (must decrease from 95 to 60 to have effect independent of pco2). When po2 drops it causes peripheral chemoreceptors to be more sensitive to blood pco2.
Inhalation reflex (Hering-Breuer reflex)
baroreceptors initiate this reflex to shut off inspiration and protect against overinflation
Hypothalamus
increases breathing rate if body is warm (works through respiratory center)
Limbic system
alters breathing rate in response to emotions (works through resp. center)
Frontal lobe and cerebral cortex
controls voluntary changes in breathing patterns. bypasses respiratory center and stimulates lower motor neurons directly.
Nervous control of respiratory system
Respiratory system includes both smooth muscles and glands. It is innervated by axons of lower motor neurons of ANS and controlled by autonomic brainstem nuclei
Nervous control of breathing muscles
innervated by lower motor neurons of somatic NS. Controlled by brainstem autonomic nuclei, cerebral cortex, and somatic nervous system. It is both a reflexive and conscious control of breathing.
F = change of P/R
change of P = pressure difference b/w atmosphere and interpulmonary pressure Patm - Palv.
R= resistance F= flow
Flow directly relates to pressure gradient and inversely relates to resistance. (if pressure gradient increases, airflow to lungs increases; if resistance increases, airflow lessens)
Resistance
factors that increase difficulty moving air. Can be altered by 1. change in elasticity of chest wall and lungs, 2. change in bronchiole diameter, or 3. collapse of alveoli.
chest wall elasticity and resistance
elasticity decreases with aging and disease, vertebral malformations, arthritis, or pulmonary fibrosis.
Bronchiole diameter and resistance
bronchoconstriction of occlusion increases resistance. Can be caused by parasympathetic activity, histamine, cold, excess mucus, or inflammation.
bronchodilation decreases resistance. Caused by sympathetic stimulation or epinephrine
collapsed alveoli and resistance
can occur if alveolar type II cells are not producing surfactant (so high surface tension of alveoli is not overcome). Important factor for premature infants when alveoli collapse with expiration. Can cause respiratory distress syndrome.
Compliance
ease with which lungs and chest wall expand. Determined by surface tension and elasticity of chest and lung.
Conditions that increase resistance to airflow
asthma (bronchiole size) pulmonary fibrosis (less compliance)
results in need for more forceful inspirations that require a high amount of energy. Can cause a 4-6 fold increase in energy needs (from 5% to 25% total energy expenditure)
tidal volume
amount of air inhaled or exhaled per breath during quiet breating
respiration rate
of breaths per minute
pulmonary ventilation
tidal vol. x respiration rate
500 mL x 12 breaths/min = 6 L/min
anatomic dead space
conducting zone space where there is no exchange of respiratory gases. about 150 mL.
alveolar ventilation
amount of air reaching alveoli per minute. deep breathing maximizes alveolar ventilation.
(tidal vol. - anatomic dead space) x respiration rate = alveolar ventilation
(500mL - 150mL)x12 = 4.2 L/min
physiologic dead space
normal anatomic dead space + any loss of alveoli. Some disorders decrease # of alveoli participating in gas exchange (pneumonia)
Spirometer
measures respiratory volume to assess respiratory health. Measures 4 volumes: tidal, inspiratory reserve, expiratory reserve, residual.
Inspiratory reserve volume (IRV)
amount of air that can be forcibly inhaled beyond the tidal volume; measure of compliance.
Expiratory reserve volume (ERV)
amount that can be forcibly exhaled beyond tidal volume; measure of elasticity
Residual volume
amount of air left in the lungs after the most forceful expiration.
4 capacities that can be calculated from respiratory volumes
inspiratory capacity, functional residual capacity, vital capacity, total lung capacity.
Inspiratory capacity (IC)
tidal volume + inspiratory reserve
Functional residual capacity (FRC)
Expiratory reserve volume + residual volume. Volume left in the lungs after a quiet expiration.
Vital capacity
tidal volume + inspiratory and expiratory volumes. Total amount of air a person can exchange through forced breathing.
Total lung capacity (TLC)
sum of all volumes, including residual volume. Maximum vol. of air lungs can hold.
Forced expiratory volume (FEV)
percent of vital capacity that can be expelled in a set period of time.
FEV1 = percentage expelled in one second
75-85% of vital capacity in a healthy person.
Maximum voluntary ventilation (MVV)
greatest amount of air that can be taken in and then expelled from the lungs in 1 minute. Breathing as quickly and as deeply as possible; can be as high as 30 L/min (compared to 6 at rest). All respiratory disorders impair this.
Partial pressure
pressure exerted by each gas within a mixture of gases, measured in mm Hg (written with P followed by gas symbol i.e. PO2). Each gas moves independently down its partial pressure gradient during gas exchange.
Partial pressure equation
total pressure x % of gas
is the driving force moving gas into liquid.
Nitrogen is 78.6% of gas in air
760 mm Hg x 78.6% = 597 mm Hg
Dalton’s law
total pressure in a mixture of gases is equal to the sum of the individual partial pressures.
Alveolar gas exchange
between blood in pulmonary capillaries and alveoli.
Po2 in alveoli is 104 mm Hg and po2 of blood entering is 40. Oxygen diffuses into capillaries and levels in alveoli remain constant as fresh air continuously enters.
Pco2 in alveoli is 40 and is 45 in blood so co2 diffuses to alveoli and continues until blood levels equal alveoli levels.
systemic gas exchange
between blood in systemic capillaries and systemic cells.
Henry’s law
at a given temperature, the solubility of a gas in liquid is dependent upon the 1. partial pressure of the gas in the air or 2. solubility coefficient of the gas in the liquid.
Solubility coefficient
volume of gas that dissolves in a specified volume of liquid at a given temp. and pressure. This is a constant that depends upon interactions between molecules of the gas and liquid
Gas solubility in water
carbon dioxide is about 24 times as soluble as O2
Nitrogen is about half as soluble as O2.
Gases with low solubility require larger pressure gradients to “push” gas into the liquid.
Decompression sickness
occurs when diver comes up to quickly. Nitrogen is forced into the blood due to the higher pressure and dissolved nitrogen will bubble out of solution while still in blood and tissues. Treated with hyperbaric oxygen chamber that increases partial pressure gradient for oxygen so additional oxygen can dissolve into plasma.
Thickness of respiratory membrane
0.5 micrometers
surface area of respiratory membrane
70 square meters
Ventilation-Perfusion coupling
ability of bronchioles to regulate airflow and arterioles to regulate blood flow.
Ventilation: changes by bronchodilation or bronchoconstriction. (ex: dilation in response to increased pco2 in air in bronchioles)
Perfusion: changes by pulmonary arteriole dilation or constriction (ex: dilation in response to decreased pco2 or increased po2 in blood).
Emphysema
Irreversible loss of pulmonary gas exchange surface area and inflammation of air passageways distal to terminal bronchioles. Causes widespread destruction of pulmonary elastic CT and decreased # of working alveoli. Causes inability to expire effectively. Mostly caused by smoking.
Diseases that decrease alveolar gas exchange
decreases # of alveoli: lung cancer
thickened respiratory membrane: congestive heart failure
changes in ventilation-perfusion couples: asthma, pulmonary embolism
Systemic gas exchange
PO2 in systemic cells is 40 mm Hg and 95 in systemic capillaries. Continues until blood po2 is 40 mm Hg and systemic cell po2 stays fairly consistent b/c o2 is delivered at same rate it is used unless engaging in strenuous activity.
PCO2 is systemic cells is 45 and 40 in capillaries. Diffusion continues until blood PCO2 is 45.
Oxygen transport
bloods ability to transport o2 depends on 1. solubility coefficient of oxygen (this is very low, and so very little oxygen dissolves in plasma) and 2.presence of hemoglobin (98% of o2 in blood is bound to hemoglobin)
Oxyhemoglobin
HbO2 - hemoglobin with oxygen bound
Deoxyhemoglobin
HHb - hemoglobin w/o bound oxygen
Pulse Oximeter
noninvasive way to measure oxygen. Applied to finger or earlobe and measures hemoglobin saturation by determining ratio of HbO2 to HHb. Normal reading hemoglobin saturation is greater than 95%
Carbon Dioxide transport
3 means of transport
- dissolved in plasma (7%)
- attached to amine group of globin portion of hemoglobin (23%)
- as bicarbonate dissolved in plasma (70%) - co2 diffuses into erythrocytes and combines with water to form bicarbonate and H ion. bicarbonate diffuses into plasma and co2 is regenerated when blood moves through pulmonary capillaries and the process is reversed.
Hemoglobin as a transport molecule
o2 attaches to iron, co2 and hydrogen ions attaches to globin. Binding of one substance causes a change in shape of the hemoglobin and changes its ability of hemoglobin to bind or release the other two substances
cooperative binding effect
each o2 that binds causes a change in hemoglobin making it easier for the next o2 to bind.
Oxygen-hemoglobin saturation curve
s-shaped, nonlinear relationship that shows large changes in saturate occur with small increases of po2. At po2 higher than 60 mm Hg only small changes in saturation occur (90% saturation) Hemoglobin saturation is about 98% at pulmonary capillaries as po2 is 104 mm Hg. Saturation can only reach 100% at pressures above 1 atm.
Altitude sickness
adverse physiologic effects from decrease in alveolar po2 and low oxygen saturation. Symptoms include headache, nausea, pulmonary edema, cerebral edema.
Oxygen reserve
o2 remaining bound to hemoglobin after passing through systemic circulation; provides means for additional o2 to be delivered under increased metabolic demands: blood leaving capillaries in active muscles are only 35% saturated as opposed to 75% in resting body. Normally only 20-25% of transported oxygen is released.
Temperature influence on O2 release from hemoglobin
elevated temp. diminishes hemoglobins’ hold on oxygen.
influence that H binding to hemoglobin has on oxygen release from hemoglobin
hydrogen ion binding causes conformational change that decreases affinity for oxygen release.
Bohr effect
H ion causing decreased affinity for oxygen release.
Presence of 2,3-BPG molecules on oxygen release from hemoglobin
these are molecules found in erythrocytes. When they bind to hemoglobin, they cause release of additional oxygen. Thyroid, epinephrine, growth, and testosterone hormones stimulate 2,3 BPG production.
Effect that Co2 binding to hemoglobin has on oxygen release
binding causes release of more oxygen from hemoglobin
Haldane effect
release of oxygen causes changing hemoglobin which increases the amount of co2 that can bind.
Shifts in saturation curve
variables that decrease oxygen affinity for hemoglobin shift right and increase shift left.
Effects of Carbon Monoxide
interferes with oxygen binding to hemoglobin because it has a stronger bond to iron. Risk of atherosclerosis is increased and decreased blood flow results in decreased nutrients and oxygen to cells. Can be treated with hyperbaric oxygen chambers.
Hyperventilation
breathing rate or depth above body’s demand. Caused by anxiety or ascending to high altitude. Causes Po2 to rise and pco2 to fall in alveoli. Additional oxygen does not enter blood and there is a greater loss of co2 resulting in hypocapnia. Hypocapnia causes vasoconstriction and less o2 to brain. May decrease H ions and if buffers cant compensate, you get respiratory alkalosis. Symptoms include fainting, numbness, dizziness, cramps, tetany, disorientation ect.
respiratory alkalosis
increased respiration elevates the blood pH beyond the normal range (7.35–7.45) with a concurrent reduction in arterial levels of carbon dioxide.
Hypoventilation
breathing too slow (bradypnea) or too shallow (hypopnea). May be caused by brainstem injury, airway obstruction, pneumonia. O2 levels decrease and co2 increase in alveoli. may result in inadequate oxygen delivery and increased hydrogen ion concentration due to high blood pco2. Symptoms include lethargy, sleepiness, headache, polycythemia, cyanotic tissue, convulsions.
hypoxemia
low blood po2
hypoxia
low oxygen in tissues
respiratory acidosis
Respiratory acidosis is a condition that occurs when the lungs can’t remove enough of the carbon dioxide (CO2) produced by the body. Excess CO2 causes the pH of blood and other bodily fluids to decrease, making them too acidic
Breathing and exercise
hyperpnea and increased cardiac output will occur to meet increased tissue needs. rate remains the same but depth increases. blood po2 and pco2 remain relatively constant. Respiratory center is stimulated by proprioceptive sensory signals, motor output from cerebral cortex, or anticipation of exercise.
