respiratory alll

goals

get O2 to cells, remove CO2(acid), acid-base balance of blood (pH)

phases of respiration & exchange of gases

1) pulmonary ventilation

2) external exchange

3) gas transport

4) internal exchange

5) exhale

pulmonary ventilation 1

inhalation/exhale

exchange between atmosphere & alveoli air sacs (site of gas exchange) [1]

external exchange

O2 diffuse from alveoli into blood Co2 vice versa

passive, no ATP, hi to lo

gas transport

hemoglobin: heme has Fe2 (assume iron), bonds 4 O2 molecules

internal exchange

O2 diffuse from blood → interstitial fluid → cells

CO2 into of blood

all require pressure gradients & no atp required

myoglobin

muscle storage of oxygen (O2)

sinuses

spaces + septum in nasal cavity

lined by cilliated cells

mucosa (trap debris)

move to oropharynx so you may expectorate

expectorate

cough out

capillaries

warm & humidify , filter air

pharynx

tube lined by mucosa, continuous with nasal cavity

“throat”

uvula+ soft palate

move up to close nasopharynx when swallow.

eustachian tube

ear’s tube opens to nasopharynx

how we connect middle ear to throat → equalizing pressure

nasopharnyx

nose throat

oropharynx

passage for food & air

see palatine tonsils

mouth throat

laryngopharynx

opens to larynx (voice)

voice box throat

adenoids

pharyngeal tonsil

throat

palatine tonsil

palate

lingual tonsil

tongue

larynx

superior to trachea & regulates air in/out of lungs

voice box

Cartilages (larynx)

Thyroid

epiglottis

cricoid.

thyroid cartilage

adam’s apple, protects cords

cricoid cartilages

encircles trachea site of tracheostomy: intubate

epiglottis

cartilage flap

protection

covers glottis & trachea in swallowing

esophagus is posterior (behind)

prevents aspiration

glottis

opening between vocal cord folds that adduct

stretch/shorten & vibrate when talking

aspiration

breathing in foreign material into the lungs,

vocal cords

connective tissue, mucosa, muscle

trachea

bronchial tree

windpipe is in mediastinum

mediastinum

space between lungs

c cartilage

in trachea

prevents collapse under negative pressure

mucuosa

innate, born with → immune related

cilia

hair cells

mucosa + cilia

trap/move debris to laryngopharynx & oropharynx

fissure

split between lobes

right & left primary bronchi

enter lungs at hilum (depression)

secondary, tertiary bronchi

lead to bronchioles → terminate in alveoli sacs

bronchioles

distal (away from center)

smooth muscle tubes → easily inflamed

right lung

3 lobes

left lung

has a cardiac notch

diaphragm

respiratory muscle

creates pressure gradients for ventilation (phrenic nerve)

phrenic nerve

stimulates diaphragm

lungs location

pleural cavity (MOST SPECIFIC, 2)

thoracic

ventral (broadest, anterior)

alveoli

site of gas exchange

elastic sacs with pores between alveoli = equal pressure in system

respiratory membrane

→ fast diffusion of gas bcos efficiency

alveoli + capillary bed (blood)

simple squamous (1 flat inner tissue) endothelium (Type 1 cell) with capillaries

type 1 cell

simple squamous (1 flat inner tissue) endothelium with capillaries

in alveiolus

alveoli lined by H2O

needed for diffusion (like interstitial fluid @ cells)

type 2 cell

make lipid/surfactant (dish soap) to break H2O’s surface tension

without it, alveoli would stick shut

oxygen in alveoli

diffuse high to low, passive transport, no energy

macrophage

white blood cells

eat

phagocytic antigen presenting cells

pleurae 1

membrane = reduce friction in respiration

surrounds lungs

1 cell layer called mesothelium

parietal (outer) layer touches thoracic cavity [1]

pleural space

makes serous fluid

visceral layer

inner layer of pleurae

folds back, touches lung

H2O goes from high to low into pleural space

oncotic pressure, reabsorbs some fluid, albumin

empyema

py= pus/infection in pleura

oncotic pressure 1

reabsorbs some fluid

pleural space into visceral/parietal pleura

albumin [1]

effusion

pleural fluid leaks outside @ lungs

apply pressure, causing atelectasis

accumulation of fluid within the pleural space

exudative vs transudative

atelectasis

collapses

transudative pleural effusion

occurs due to increase hydrostatic pressure or low plasma oncotic pressure

EX: CHF, cirrhosis, nephrotic syndrome, PE, hypoalbuminemia

low in protein and LDH

hypoalbuminemia

transudative pleural effusion

low blood protein → nothing to keep H2O in blood → H2O leaks into tissue

exudative pleural effusion

infection

occurs due to inflammation (caps) and increased capillary permeability

EX: pneumonia, cancer TB, viral infection, PE, autoimmune

FLUID ESCAPES

high in protein and LDH

pleurae 2

serous membrane = reduce friction in respiration

surrounds lungs

1 cell layer called mesothelium

parietal (outer) layer touches thoracic cavity [2]

pleural space

makes serous fluid

visceral layer

inner layer of pleurae

folds back, touches lung

H2O goes from high to low into pleural space

oncotic pressure, reabsorbs some fluid, albumin

empyema

py= pus/infection in pleura

oncotic pressure

reabsorbs some fluid into cap

pleural space into visceral/parietal pleura

albumin

effusion

pleural fluid leaks outside @ lungs

apply pressure, causing atelectasis

accumulation of fluid within the pleural space

exudative vs transudative

atelectasis lung

collapses

transudative pleural effusion

occurs due to increase hydrostatic pressure or low plasma oncotic pressure

EX: CHF, cirrhosis, nephrotic syndrome, PE, hypoalbuminemia

low in protein and LDH

hypoalbuminemia

transudative pleural effusion

low blood protein → nothing to keep H2O in blood → H2O leaks into tissue

exudative pleural effusion

infection

occurs due to inflammation (caps) and increased capillary permeability

EX: pneumonia, cancer TB, viral infection, PE, autoimmune

FLUID ESCAPES

high in protein and LDH

hydrostatic pressure

high to low, passive transport

pushes fluid from capillaries into pleural space

pulmonary ventilation 2

act of breathing (inhale/exhale)

driven by high-low gradients

& diaphragm [2]

atmospheric pressure (P-atm)

force exterted by gasses @ a surface (mmHg)

1 atm =760 mmHg

must be higher than inside lungs = gradient

intraalveolar/P-alv

intrapulmonary = pressure in lungs

must be lower than atmosphere for air to flow into lungs

0 atm=it equalizes with atmosphere at end of inhale/exhale

intrapleural/ P-ip

around cavity @ lungs

must be lower than p-alv

If not lower than P-alv, lungs cannot inflate

inhalation gradient

P-atm > P-alv > P-ip

exhalation

as diaphragm relaxes/domes up, pressure gradient reverses

passive

thoracic volume decreases & p-alv pressure increases

exhalation, gradient of airflow out

thoracic volume decreases & p-alv pressure increases

inhalation

inspire

active = diaphragm contracts down & expands thoracic cavity

thoracic volume increases → causes p-atm higher vs p-alv pressure lower = h-low gradient = flow in

chest volume up, lungs pressure down

boyle’s law

pressure and volume are inverse

end of inhale, end of exhale

no gradient

patm=palv

atelectasis define

collapsed lung/incomplete expansion

no gradient for expansion if P-ip >= p-alv

pleura >= lung

pneumothorax

air in chest around lungs

pleura >= lungs

spirometry

measure breathing volume (mL)

tidal volume

amouunt of air entering lungs during quiet/rest breathing

@500 mL

expiratory reserve

amount you can forcefully exhale past normal tidal exhalation

residual volume

air left in lungs after max exhale & this prevents alveoli collapse

vital capacity

max volume of air that can be moved in or out

respiratory rate

#breaths/min

controlled by medulla & pons in brainstem → sleep

adjust based on chemoreceptors

chemoreceptors

in aorta

sense dissolved CO2 (acid)/O2 & pH

respiratiory rate adjusted based on these : 12-18/min normal

go to carotids → medulla → diaphragm

increased CO2

more diaphragm contracts → more breathing

blood ph

7.35-7.45, change at most .1

buffer systems resist pH changes by reducing or adding H+ ions to a system

CO2 transport

bicarbonate buffer system

70% of CO2 transported as bicarbonate (HCO3-) = kidneys

Bicarbonate/HCO3 jobs

soaks it up, sponge

buffers blood

removes excessive H+ ions

keep pH stable

transport CO2 to lungs

hypercapnemia

CO2 increases via increased muscle use, metabolism, hypoventilation

leads to acidosis

hypoventilation

not breathing enough

pulmonary acidosis

H+ ions increase = pH decrease, too acidic

CO2 increase (hypercapnemia) via increased muscle use, metabolism, or hypoventilation

increase pH

rate & depth of ventilation via communication from medulla to diaphragm increase to expel more CO2 & thus decrease H+ ions in blood

alkalosis

pH increase

Co2 decreases (hypocapnemia) due to hyperventilation → less H+ ions in blood

too basic

traumatic pneumothorax

puncture wound in chest wall to get air in chest around lungs

spontaneous pneumothorax

hole in lung causes air to be in cavity