Physio 6102 Respiratory System

Functions of Respiratory System (6)

1. provides body with O2

2. eliminates CO2

3. regulates pH [H+] in blood

4. speech via vocal cords

5. defense against microbes

6. influences chemical messengers in blood

components of respiratory system

tubes into lungs, right and left lungs, alveoli, chest + diaphragm moves air into/out of lungs

respiratory cycle

one inspiration, one expiration

pathway of air during inspiration

upper airways to conducting zone to respiratory zone

upper airways

nose/mouth and pharynx

air into larynx, food into espohagus

upper airway diseases

inflammation from common cold/rhinitis

upper airway constriction (adenotonsillar hypertrophy- obstructive sleep apnea or choking)

air flow in conducting zone

bulk flow into trachea to 2 bronchi

into bronchioles (shorter/smaller tubes)

bronchi diameter controlled by

cartilage

bronchiole diameter controlled by

smooth muscle

respiratory zone composed of

alveoli (like tree)

3 functions of conducting zone

1, low-resistance pathway for airflow

2. warms + moistens air

3. defense against microbes/foreign particles

three defense mechanisms against foreign matters in conducting zone

1. surrounding cells have cilia, beat toward pharynx

2. cells secrete mucus to trap particles → pharynx

3. macrophages engulf foreign particles

conducting zone dysfunctions

cystic fibrosis + asthma

respiratory zone contains

7 branchings of tree: increases surface area for gas exchange

bronchioles + alveoli

gas exchange in respiratory zone

diffusion

cystic fibrosis

genetic CFTA Cl- channel mutation

mucus secretion dehydrated, thickens

causes obstructive blockages in breathing and bacterial accumulation

histology of respiratory zone

terminal bronchiole → respiratory bronchioles → alveoli

conducting zone doesn’t do

gas exchange

blood vessels and airway relationship

pulmonary artery and vein out of/into heart

pulmonary pressure LOW as compared to systemic

pulmonary artery hypertension

narrows, hypoxia, smooth muscle around artery constricts, difficult for right heart to pump into lungs

structure of alveolus

hollow sac open to airways

one cell-thick walls, secrete surfactant

two types of alveoli

type I: squamous epithelia alveolar: flat

type II: surfactant-secreting alveolar cells: cubical

oxygen must diffuse through 4 layers

1. thin layer of fluid lining alveolus

2. alveolar epithelium

3. alveolar and blood capillary basement membranes + interstitial connective tissues

4. blood capillary endothelium

air travel sequence in inhalation

pharynx → larynx → trachea → bronchi → alveoli

alveoli dysfunction

ARDS (acute respiratory distress syndrome) and sepsis

cytokine release, neutrophil infiltration, alveolar-capillary leak, edema

ARDS caused by

inhaled pathogens (COVID/bacteria)

lungs to chest wall relationship

thorax: closed compartment separated from abdomen by diaphragm

thoracic cage: spinal column, ribs, sternum, internal/external intercostal muscles

lungs to pleural sac relationship

lung surrounded by pleural sac

attached to lung by connective tissue and thoracic wall/diaphragm muscle

pleural sac

contains thin layer of intrapleural fluid (lubricates surfaces)

pressure changes in fluid causes changes in lung volume

how to lung surface and thoracic wall move

in/out together

ventilation

exchange of air between atmosphere and alveoli (high to low pressure)

air flow proportional to, inversely prop. to

pressure difference, resistance to flow

change in pressure: which two points

alveoli - atmosphere pressures

air flow equation

change in P/resistance

inspiration pressures

Palv < Patm

expiration pressures

Palv > Patm

P atm (relative)

760 mmHg, considered to be 0

what causes pressure change in alveoli

change in lung volume

which gas law underscores change in lung volume

Boyle’s law: constant temperature, volume and pressure are inverse

this drives air flow into/out of lungs

when lung volume increases, what happens to alveolar pressure

decreases (and vice versa)

what determines lung volume

compliance/ease of lung stretching

difference in pressure inside vs outside lungs

pressure inside lungs is, outside is

alveolar pressure, intrapleural pressure (in pleural sac)

transpulmonary pressure

alveolar P - intrapleural P

determinant change in lung volume: across the lung

trans-chest-wall pressure

Pip - Patm

intrapleural pressure is always

-4: subatmospheric

chest and pleural pressures are

opposing

three pressure changes in respiratory cycle

between breaths: Ptp is 4 to expand lungs

inspiration: Ptp increases to increase lung volume

expiration: Pip increases, Ptp decreases to passively recoil lungs

positive TP means

lungs contain some air (ALWAYS)

rupture of lung/chest wall results in

pneumothorax: Pip = 0 so Ptp = 0

lung collapses, rip cage expands

diaphragm + rib cage movement in respiration

inspiration: diaphragm descends, intercostal muscles elevate

expiration: diaphragm ascends, intercostals depress

inspiration events

diaphragm + intercostals contract

thorax expands

Pip decreases

Ptp increases

Palv decreases to move air inside

is there muscle connected directly to lungs?

NO: connected to pleural wall

when does inspiration end?

when Palv = Patm

what also contracts in large inspiration

other accessory muscles like scalenes

events during expiration

diaphragm + intercostals relax

chest wall recoils

Pip increases, Ptp decreases (return to preinspiration values)

lungs passively recoil to original dimensions

alveoli compress, Palv increases

air flows from lungs → atmosphere

air flows in expiration until

Palv = Patm

in expiration Pip is always, Ptp is always

subatmospheric, positive

so some air left in lungs

explain this diagram

talk about changes in each pressure

lung compliance definition

magnitude of the change in lung volume produced by a given change in Ptp

change in volume/Ptp

inverse of stiffness

lower lung compliance resilts in _ increase in volume for given increase in Ptp

less

patients with low compliant lungs:

breathe more shallowly, more rapidly for adequate ventilation

factors determining lung compliance

elasticity of connective tissue, surface tension at air-water interface in alveoli

clinical significance of lung connective tissue

pulmonary fibrosis

atelectasis/pneumothorax

emphysema/COPD

pulmonary fibrosis

ECM accumulation, scarring, decreased elasticity and compliance (more work to inflate rigid alveoli)

atelectasis/pneumothorax

decreased lung compliance

emphysema/COPD

elastic recoil property damage, high compliance, hard to exhale excess air

air sacs of the lungs damaged/enlarged, can be caused by smoking

surface tension

attractive force: pulls surface molecules together at air-liquid interface: maximize surface area

surface tension of PURE water in alveoli

difficult to expand, collapse: more energy to overcome surface tension + elastic lung tissue properties

purpose of surfactant

reduces surface tension to pull water molecules together, reduces surface tension too increase compliance

secreted by type II cells lining alvelo

what is surfactant

phospholipid/protein mixture, forms monolayer between air and water

mechanism of surfactant production

deep breath stretches type II cells, induces surfactant secretion

law of laplace

pressure = 2(surface tension)/radius

pressure prop. to ST, inverse to alveolus radius

why is surfactant important

stabilization of differently-sized alveoli to prevent collapse of small or over-expansion of large alveoli

based on radius size

respiratory-distress syndrome of newborn

surfactant deficiency, low compliance, increase work of breathing

mechanical ventilation + artificial surfactant administration

main determinant of airway resistance

tube radius (resistance inversely prop. to 4th power of airway radius)

physical factors that affect airway radius

transpulmonary pressure distends bronchioles

elastic connective tissue link outside of airways to alveloar tissue (lateral traction)- stretched during inspiration

neural + chemical factors that affect airway radius

control smooth muscle contraction/relaxation

epinephrine relaxes, leukotrienes contract

abnormal airway resistance in asthma

inflammation of airways (allergy), smooth muscle hypersensitive to environmental changes

asthma treatments

leukotriene inhibitors/ glucocorticoids for anti-inflammation
bronchodilator drugs for epinephrine to relax

chronic bronchitis

xs mucus in bronchi, chronic inflammation in airways to decrease diameter, increase resistance

lung volume measures

tidal volume:

inspiratory reserve volume

expiratory reserve volume

residual volume

lung capacities

tidal volume (Vt)

volume entering/leaving lungs per breath (500 mL)

inspiratory reserve volume (IRV)

max air above TV in deepest inhalation (3000 mL)

expiratory reserve volume (ERV)

max air exhaled beyond Vt (1200 mL)

residual volume (RV)

air in lungs after max exhalation (1200 mL)

lung capacities

vital capacity, functional residual capacity, total lung capacity

vital capacity (VC)

max air a person can expire after maximal inspiratory (4700 mL)

Vt + IRV + ERV

functional residual capacity (FRC)

volume of air remaining in lungs after quiet expiration

ERV + RV

total lung capacity (TLC)

max amount of air lungs can contain

RV + IRV + ERV + Vt

forced expiratory volume in 1 sec

fraction of forced VC exhaled in one sec, 80% FVC

FEV1 in obstructive long diseases

decreased FEV1/FVC, increased resistance to expiration

FEV1 in restrictive lung diseases

decreased VC

normal or increased FEV1/FVC

respiratory minute ventilation

TV x respiratory rate

Ve = Vt x f

500 mL/breath x 12 breaths/min = 6000 mL/min

not ALL inhaled air for blood-gas exchange due to dead space

how much new atmospheric air reaches alveoli/breath

350 mL

alveolar ventilation

total volume of fresh air entering alveoli per minute

(TV - dead space) x respiratory rate
Va = (Vt - Vd) x f

4200 mL/min

to increase alveolar ventilation, what is more effective?

increase TV more effective than increase in respiratory rate

same minute ventilation, different alveolar ventilation

because dead space increases

two types of dead space

alveolar dead space: alveolar air that does not exchange with blood

physiologic dead space: anatomical + alveolar dead space

steps in respiration

ventilation: exchange of air b/w atmosphere and alveoli (bulk flow)

exchange of O2 and CO2 b/w alveolar air and blood in lung capillaries: diffusion

transport of O2 and CO2 through pulmonary and systemic circulation by air flow

exchange of O2 and CO2 b/w tissue capillary blood and cells in tissues by diffusion

cells use O2, produce CO2

pressure exerted by gas proportional to

temperature and gas concentration