KAAP310 EXAM 2 - Respiratory Content

functions of respiratory system

gas exchange, communication, olfaction, acid-base balance, blood pressure regulation, platelet production, blood/lymph flow, blood filtration, expulsion of abdominal contents

conducting zone

consists of passages that serve only for airflow

from nostrils to major bronchioles - walls of passages are too thick for adequate oxygen diffusion from air to blood

respiratory zone

consists of alveoli and other gas exchange regions of distal airway

upper respiratory tract: airway from nose to larynx

lower respiratory tract: trachea through lungs

nasal cavity epithelia

begins with vestibule - stratified squamous

past vestibule, ciliated pseudostratified columnar epithelium with ciliated cells and goblet cells

small area has olfactory epithelia which have immobile cilia

oral cavity epithelia

stratified squamous epithelia (mostly nonkeratinized, but can be keratinized in hard palate and gingiva)

protects against mechanical stress from chewing and food

pharynx epithelia

nasopharynx: pseudostratified columnar epithelium to filter/humidify air

oropharynx and laryngopharynx: stratified squamous epithelium to protect against abrasion

larynx epithelia

above vocal cords: stratified squamous epithelium to protect cords from mechanical stress

below vocal cords: pseudostratified columnar ciliated epithelium to move mucus and debris

trachea epithelia

pseudostratified ciliated columnar with goblet cells to move mucus upward toward pharynx to clear inhaled particles

cell types of alveoli

squamous type I alveolar cells, great type ii cells, and alveolar macrophages (dust cells)

squamous type i cells

cover 95% of surface area and allow for rapid gas diffusion

great type ii cells

cover 5%, round to cuboidal shape

repair alveolar epithelium when squamous cells are damaged

secrete pulmonary surfactant that prevents alveolar/bronchiole collapse when exhaling

alveolar macrophages

wander lumens of alveoli and CT between them and phagocytize dust particles that escape entrapment by mucus

pulmonary blood vessels and alveoli relationship

pulmonary arteries carry deoxygenated blood to lungs - branch extensively and form networks around each alveolus

capillary walls and alverolar walls form respiratory membrane - thin membrane allowing for rapid gas diffusion

structure of respiratory membrane

barrier between alveolar air and blood

squamous alveolar cell, squamous endothelial cell of capillary, and shared basement membrane

diameter of single erythrocyte

actions of respiratory muscles during inspiration

sternocleidomastoid elevates sternum

scalene fix/elevate ribs 1-2

external intercostals elevates ribs 2-12 and widens thoracic cavity

pectoralis minor elevates ribs 3-5

internal intercostals aid in elevating ribs

diaphragm descends and increases depth of thoracic cavity

actions of respiratory muscles during expiration

internal intercostals depress ribs 1-11 and narrows thoracic cavity

diaphragm ascends and reduces depth of thoracic cavity

rectus abdominis depresses lower ribs, pushes diaphragm upwards by compression abdominal organs, assisted by external oblique

brainstem respiratory centers

ventral respiratory group, dorsal respiratory group, pontine respiratory group

ventral respiratory group

primary generator of respiratory system

elongated neural network in medulla

In quiet breathing, the I neuron circuit fires for about 2 seconds at a time to contract muscles to enlarge thoracic cage and cause inspiration - once I neurons stop firing, E neurons begin firing

eupnea

normal respiration, about 12 breaths per minute

dorsal respiratory group

modifies basic respiratory rhythm, extends length of medulla between VRG and canal of brainstem

modulates the VRG's activity by receiving input from several sources (PRG, chemosensitive center in medulla, chemoreceptors in major arteries, stretch/irritant receptors in airways, higher brainstem centers)

pontine respiratory group

receives input from higher brain centers and issues output to DRG and VRG

hastens or delays transition from inspiration to expiration - adapts to circumstances like sleep, exercise, vocalization, or emotional responses

central chemoreceptors

brainstem neurons that respond to changes in pH of CSF

on each side of medulla

ensures stable CO2 level

peripheral chemoreceptors

in carotid and aortic bodies of large arteries that respond to O2, CO2, and pH content

glossopharyngeal (carotid bodies) and vagus (aortic bodies) nerves enter medulla and synapse with DRG neurons

stretch receptors

found in smooth muscle of bronchi, bronchioles, and visceral pleura

respond to inflation of lungs and signal DRG by vagus nerves

excessive inflation triggers the inflation reflex, which strongly inhibits the I neurons and stops inspiration

irritant receptors

nerve endings amid epithelial cells of airway

respond to irritants

transmit signals via vagus to DRG, and DRG returns signals to respiratory and bronchial muscles, resulting in protective reflexes such as bronchoconstriction, shallow breathing, apnea, and coughing

neural pathway for voluntary control of respiration

originates in motor cortex

output neurons send impulses down corticospinal tracts to integrating centers in spinal cord, bypassing brainstem centers

holding one's breath raises CO2 level of blood until breaking point is reached when automatic controls override

relationship between airflow, pressure, and resistance

airflow is directly proportional to pressure difference

airflow is inversely proportional to resistance

how and why do intrapulmonary pressures change relative to atmospheric pressure during inhalation

during inspiration, diaphragm contracts and flattens, increasing volume of lungs which decreases intrapulmonary pressure

because air flows from high to low, pressure difference causes air to flow into lungs (atmospheric pressure - 760 mmHg, intrapulmonary pressure 758 mmHg)

boyle's law

the pressure of gas is inversely proportional to its volume

if lung volume increases, intrapulmonary pressure decreases and vice versa

charles's law

the volume of gas is directly proportional to its absolute temperature

inhaled air is warmed to 37C by the time it reaches the alveoli, and the inhaled volume will expand and contribute to the inflation of the lungs

bronchodilation

widening of bronchi

increases airway diameter -> decreases resistance to airflow -> improves ventilation

triggered by sympathetics such as epinephrine during exercise or stress

bronchoconstriction

narrowing of bronchi

increased airway resistance -> decreased ventilation

triggered by parasympathetics, allergens, irritants

pulmonary compliance

the lung's ability to stretch and expand

high compliance -> lungs inflate easily -> better ventilation

low compliance -> lungs are stiff -> reduced ventilation

can be affected by age, disease, or structural lung tissue damage

alveolar surfactant

lipid-protein mixture produced by type ii alveolar cells that reduce surface tension inside alveoli

prevents alveolar collapse -> increases compliance and reduces work of breathing -> better ventilation

not enough surfactant -> alveoli collapse -> poor ventilation

composition and partial pressures of atmosphere

Nitrogen - 78.6%, 597 mmHg

Oxygen - 20.9%, 159 mmHg

Carbon dioxide - 0.04%, 0.3 mmHg

Water - 0.5%, 3.7 mmHg

total pressure = 760 mmHg

dalton's law

total atmospheric pressure is a sum of the contributions of these individual gasses (partial pressures)

i.e., average atmospheric pressure is 760 and oxygen is 20.9%... 0.209 x 760 = 159 mmHg <- pp of oxygen

alveolar air

lower nitrogen, lower oxygen, higher water, and higher carbon dioxide

alveolar air is humidified, so water is higher

freshly inspired air is combined with leftovers, so oxygen is diluted and CO2 is enriched

alveolar air exchanges O2 and CO2 with blood, so O2 is lower and CO2 is higher

gas exchange and water solubility

air in alveoli is in contact with the film of water covering the alveolar epithelium, so for oxygen to get into the blood, it must dissolve in water and pass through the respiratory membrane

diffusion only works for dissolved substances

four variables determining rate of oxygen loading and carbon dioxide unloading

partial pressure gradients of the gasses, solubility of the gasses, thickness of respiratory membrane, surface area of respiratory membrane

partial pressure gradients of the gasses

O2: higher pp in alveoli (100mmHg) vs lower in capillaries (40 mmHg) so O2 diffuses into the blood

CO2: higher in capillary blood (45 mmHg) than alveoli (40 mmHg) so CO2 diffuses out of the blood

greater gradient = faster diffusion

solubility of the gasses

CO2 is 20x more soluble in water than O2, so O2 needs a steeper pressure gradient to move effectively

thickness of respiratory membrane

thicker membrane slows diffusion

thin=faster exchange

normally 0.5 um thick

surface area of respiratory membrane

if SA decreases, gas exchange efficiency drops

more surface area = more exchange opportunities

ventilation-perfusion coupling

lungs adjust ventilation so that air is directed to best-perfused parts of lungs

if part of lung is poorly ventilated, oxygen would have a low pp, which stimulates vasoconstriction and reroute the blood to better-ventilated areas to pick up more oxygen

increased ventilation raises the local blood oxygen pp, and stimulates vasodilation, increasing blood flow to that region

two modes of oxygen transport in blood

98.5% of O2 is bound to hemoglobin, and each hemoglobin can carry up to 4 O2 molecules

1.5% of O2 is dissolved in blood plasma, but is the only portion which contributes to pp of oxygen, which drives diffusion

oxyhemoglobin dissociation curve

at low PO2, the curve rises slowly, then there is a rapid increase in oxygen loading as PO2 rises

-when the first heme group binds O2, hemoglobin changes shape that facilitates uptake of second, third, and fourth, which explains the rising midportion of curve

at high PO2 levels, the curve levels off because the hemoglobin reaches 100% saturation

three modes of CO2 transport

90% is hydrated to form carbonic acid, which dissociates into bicarbonate and hydrogen

5% binds to amino groups of plasma proteins and hemoglobin to be transported

5% is carried in blood as dissolved gas

carbaminohemoglobin

hemoglobin bound to carbon dioxide on its polypeptide chains

how carbonic anhydrase and chloride shift help load CO2

CO2 enters RBCs from tissue fluids

CAH converts CO2 + H2O -> H+ and HCO3-

Bicarbonate is transported out of RBC into plasma to avoid buldip

Chloride ions move into RBC as bicarbonate exits to maintain electrical neutrality -> keeps reaction going by removing its products and ensuring continued CO2 uptake

H+ binds to hemoglobin as well, which prevents dangerous pH drop

-Bohr effect - low pH + high CO2 = more O2 unloading

four mechanisms that adjust amount of oxygen unloaded by hemoglobin

lower PO2 in tissues, higher temperature, Bohr effect, and BPG

lower PO2 in tissues

lower PO2 in tissues -> more O2 unloading from hemoglobin

oxygen diffuses from high to low, so more active tissues creates a steeper gradient, pulling in more O2

higher temperature

higher temperature = more O2 unloading

active tissues generate heat -> hemoglobin releases O2 more readily

Bohr effect

lower pH reduces hemoglobin's affinity for O2 -> more O2 release in acidic environments where cells are metabolically active

BPG

BPG is produced by RBCs when tissues are active (hypoxia, fever, high altitude)

BPG binds to hemoglobin and reduces its affinity for O2 -> promotes O2 unloading

three factors that stimulate chemoreceptors

CO2 levels, pH levels, and O2 levels

CO2 and chemoreceptors

high CO2 -> both central and peripheral chemoreceptors -> increases breathing rate and depth

pH levels and chemoreceptors

low pH -> both central and peripheral chemoreceptors -> increases breathing rate and depth to expel CO2 and reduce acid

O2 levels and chemoreceptors

low O2 -> mainly peripheral chemoreceptors -> increases breathing rate and depth

how exercise increases respiration

Increased CO2 decreases pH, which trigger chemoreceptors to send signals to respiratory centers to increase breathing rate and depth

Increased O2 demand increases ventilation -> PO2 in lungs decrease due to increased consumption in muscles, which is sensed by peripheral chemoreceptors and increase RR and TV

Epinephrine increases ventilation by stimulating b-adrenergic receptors in smooth muscle of airways, leading to bronchodilation