human physiology: the respiratory system

inspiration and expiration

inspiration allows O2 to enter the lungs and expiration allows acidic CO2 to leave the lungs

gas transportation

is a function of the cardiovascular system! the respiratory system is responsible for ventilation and gas exchange

mucosa

layer of ciliated epithelial cells and goblet cells that secrete mucus, which traps inhaled particles that enter the airways; mucosa membranes are found in the nose, trachea, bronchi, and bronchioles

mucociliary escalator

movement of mucus and trapped particles along the respiratory tract towards the pharynx via cilia motion; once in the pharynx, globs of goo can be swallowed or spit out

periciliary fluid

watery fluid that negotiates movement of mucus along the respiratory tract; mucus clogs airways if preiciliary fluid is deficient because the mucus is obnoxiously thick

function of the nose

filter, warm, and humidify incoming air through to air turbulence created by spiral nasal conchae structures; turbulent air interacts with mucosa and helps catch any particles

pharynx

extends from the nasal and oral cavities to the esophagus and the larynx; passageway for food and air and also helps amplify speech sounds

larynx (voice box)

allows air, but not fluid or food, into the rest of the airways thanks to the epiglottis; also houses vocal cords, which vibrate to produce noises when air passes over them

trachea (windpipe)

conveys air from the larynx to the lungs and is composed of strong cartilage rings to promote airflow and prevent collapse

cystic fibrosis cause

CFTR channel for cl- ions is mutated. it is not in the plasma membrane and causes a decrease of cl- secretion, which leads to less na+ and water movement into periciliary fluid. less juice causes the mucus to thicken and clog the airways, also leading to high risk for bacterial infections. long term effects are difficulty breathing, decreased quality of life, and lung disease.

pleural cavity

composed of parietal (outer) pleura and visceral (actually on the lungs) pleura linings: intrepleural fluid circulates around the lungs as lubricant, which reduces friction and allows for easy movement during respiration

lung inflammation

pleurisy is inflammation and pain due to lung friction between the pleural linings; pleural effusion is the progression of pleurisy and is characterized by excess fluid accumulating in the pleural space

smooth muscle in lungs

allows bronchioles to regulate diameter of tubes, which influences airflow to the alveoli as needed; epinephrine and norepinephrine on b2 receptors cause relaxation (bronchodilation) during exercise and ach from parasympathetic neurons return your ventilation level to normal after exercise via bronchoconstriction

asthma

a respiration disorder characterized by airway inflammation, airway hypersensitivity, and airway obstruction due to spasms of walls of bronchi and bronchioles; albuterol is a b2 adrenergic agonist, stimulating bronchodilation as a way to open airways

structure of pulmonary circulation

high blood flow with low resistance to receiving entire cardiac output from the right side of the heart to be oxygenated before being sent to the left side to the aorta! vessels have large diameters and thin walls and are very compliant — perfect ingredients for gas exchange at the alveoli

ventilation

mechanical flow of air into and out of the lungs based on atmospheric, alveolar, and intrapleural (pleural cavity) pressure

inspiration phase of breathing cycle

diaphragm contracts downwards, increasing the volume of the lungs and decreasing alveolar pressure to 748 mmHg and intrapleural pressure to 754 mmHg. the drop in pressure in the lungs pulls air from the external to the internal environment, similar to how air is pulled into a tube when a syringe is pulled back

expiration phase of breathing cycle

alveolar pressure is greater (762 mmHg) than atmospheric pressure (constant at 760 mmHg); expiration is the result of elastic recoil of thoracic wall and lungs, which spring back and send air outward after being stretched due to intake of air during inhalation

expiration muscles

abdominal muscles and internal intercostals compress organs and pull the ribs downward respectively → the ribcage is pulled down and the diaphragm is forced up in active expiration during intense exercise; in a resting state, expiration is passive thanks to elastic recoil

inspiration muscles

the diaphragm is the floor of the thoracic cavity and flattens during inspiration via innervation from phrenic nerves to produce a pressure difference in the alveolar space and effectively pull air in; the external intercostals extend the ribs outwards and upwards to increase the volume of thoracic cavity and space for lung expansion and decrease internal pressure; sternocleidomastoid and scalene muscles help pull air in forcefully during exercise by elevating the sternum and the ribs to create a stronger inward pull on external air into the lungs; inspiration is always an active process due to muscle contraction

surfactant

a mixture of lipids and proteins that decreases cohesive forces in water-air base in alveoli, causing a decrease in surface tension and an increase in lung compliance

lung compliance

the freedom of the lungs to expand easily due to elasticity and surface tension of alveoli; low compliance (bad) is caused by pulmonary edema, scar tissue, or deficiency in surfactant

airflow

F = pressure gradient P/resistance to airflow R: dilation and contraction of smooth muscle innervated by the sympathetic and parasympathetic ANS respectively influences the degree of airway resistance and therefore how much airflow we have

chronic obstructive pulmonary disease (COPD)

respiratory disorder featuring chronic/recurrent obstruction of airflow and increased airway resistance due to alveolar wall damage (emphysema), excessive mucus secretion (chronic bronchitis), or smoking history

law of laplace

pressure in the alveoli P = 2T surface tension of sphere / r radius of sphere; in cases of no surfactant, the pressure in a small alveolus would be greater than the pressure in a larger alveolus, so the small one would deflate into the larger one (alveolar collapse)

role of surfactant in alveolar pressure distribution

the pressure is maintained in the bundle of alveoli and the little one does not collapse; occurs due to small alveoli having more surfactant compared to large alveoli, which equalizes the surface tension in relation to the radius of the small alveolus. by the law of laplace, pressure in the small and large alveoli are equivalent and airflow is unbiased.

ventilation-perfusion matching

maximizes gas exchange via input from CO2 and O2 chemical local mediators

ventilation > perfusion

excess ventilation causes low levels of CO2 and excess O2, so the bronchiole constricts to decrease airflow to match the lower level of blood flow; pulmonary arterioles vasodilate to better distribute O2 stores

perfusion > ventilation

acidic excess CO2 conditions cause bronchodilation to bring in more O2 and pulmonary arterioles vasoconstriction to send the blood to areas of the lung that have adequate O2 as matching is not always perfect due to the effects of gravity

eupnea

normal pattern of quiet breathing

tidal volume

vol of air inhaled or exhaled during a single breathing cycle under resting conditions; 500mL in regular adults

lung volumes and capacities

volume assesses lung function: tidal volume, IRV, ERV, and residual volume

lung capacity is the combination of lung volumes like inspiratory capacity, residual capacity, and vital capacity

v-dot = tidal volume x respiratory rate

residual volume

keeps alveoli partially inflated and ready to receive air; residual air vol get cycles in and out but residual volume stays constant

COPD and residual volume

residual volume overtakes room in lung for other capacities and bronchitis and emphysema prevent you from getting rid of RV; you essentially lack usable air even though total volume might be similar

dalton’s law of partial pressure

each gas in a mixture exudes its own pressure in proportion to its volume as though no other gases were present; in lungs, the pressure of gases N, O2, CO2, and other gases sum to 1 atm

exchange of O2 and CO2

occurs passively via diffusion between alveolar air and pulmonary blood by following partial pressure gradient; if there is a greater difference, diffusion of the specific gas occurs faster

pulmonary gas exchange

diffusion of O2 from air in the alveoli of the lungs to blood in pulmonary capillaries and diffusion of CO2 in the opposite direction; both gases diffuse independently of each other according to their respective concentration gradients

exercise and O2 exchange

the pressure gradient of O2 from inside the alveoli to inside the pulmonary capillaries is greater during exercise bc muscles are constantly using existing O2 for activity; blood flow and cardiac output is also drastically increased, so the rate of O2/CO2 diffusion also increases, but only to a certain point if gaseous equilibrium is not maintained during activity

systemic gas exchange

exchange of O2 and CO2 between systemic capillaries and tissue cells: tissue cells constantly produce CO2 as a byproduct of metabolic activity, so CO2 diffuses into the capillaries from the tissues as O2 goes into the tissues to supply them with oxygen for metabolic activity (once again respective concentration gradients)

factors that affect rate of gas exchange

partial pressure differences of the gases (greater = faster, less = slower), surface area available for gas exchange (less area due to emphysema → less room for gas exchange → slower process), diffusion distance (contracted capillaries have slower blood flow so slower gas exchange), and molecular weight and solubility of the gases

net gas exchange in respiratory membrane

O2 is lighter than CO2 so it diffuses quicker, but CO2 has a greater solubility (24x); net outward diffusion of CO2 is about 20x faster than infusion of O2, so slower than normal diffusion typically leads to hypoxia (lack of O2) before hypercapnia (excess of CO2)

oxygen transport

99% is transported in erythrocytes thanks to hemoglobin as O2 does not dissolve easily in watery solutions (like the blood plasma)

hemoglobin structure

globin is made of 4 polypeptide chains and a heme unit, the red pigment with iron at the center for binding to oxygen, is attached to each chain; each hemoglobin molecule can bind 4 oxygen molecules

cooperativity in the oxygen-hemoglobin dissociation curve

when an O2 molecule binds to a subunit of hemoglobin, the other hemoglobins undergo a conformational change that increases affinity of the hemoglobin for O2; it gets progressively easier for additional O2 molecules to bind to hemoglobin; the greater the Po2, the more O2 binds to hemoglobin until 100% O2 saturation is achieved; high saturation is achieved anywhere between Po2 of 60-100 mmHg, allowing for elite performance even at high altitudes

factors that affect affinity of hemoglobin for oxygen

high acidity (blood pH is low), high Pco2 (causes low blood pH), temp (dissolved gases leave solution at higher temps), and high levels of BPG

carbon monoxide poisoning

CO binds to heme on hemoglobin just as O2 does but with a MUCH higher binding affinity; CO displaces O2 and you quickly become fatally hypoxic