Trachea

conect larynx to lungs

pseudostratified ciliated columnar epithelium

blood from bronchial

Bronchi

has smooth muscle & cartilage

pseudostratified ciliated columnar

blood from bronchial

no cartilage

end of conducting division

simple cuboidal

blood from bronchial

no cartilage

simple cuboidal & simple squimous

blood from pulmonary

has alveoli

no cartilage

simple squimous

blood from pulmonary

last division of resperatory division

no cartilage

simple squamous

blood from pulmonary

V_E= tidal volume X respiratory rate

V_T= V_D+V_A

total volume is dead space + alveoli

alveolar ventilation = V_A X respiratory rate

alveolar ventilation = (V_CO2)/(P_aco2)

total volume of gas after a max inspiration

RV+ERV+V_T+IRV

Vital Capacity

max volume that can be expired after a max inspiration

ERV+V_T+IRV

Inspiratory Capacity

max gas that can be inspired starting from FRC

IC=V_T+IRV

Functional Residual

gas in lungs after a normal expiration

FRC=ERV-RV

parasympathetic:

ACH

contracts smooth muscle, bronchoconstriction

Sympathetic

relaxes smooth muscle

Bronchodilation

EP/NE react by β2 adrenergic

obstructive lung disease

TLC

FRC

RV

FVC

FEV1

FEV1/FVC

lung compliance

lung resistance

more airway resistance (asthma)

smooth muscle more sensitive to stimulus

(trouble breathing out)

TLC: up

FRC: up

RV: up

FVC: down

FEV1: down

FEV1/FVC: down

lung compliance: normal or up

lung resistance: up

restrictive lung disease

TLC

FRC

RV

FVC

FEV1

FEV1/FVC

lung compliance

lung resistance

cant expand completely

low vital capacity, low resting lung volume

(trouble breathin in)

TLC: down

FRC: down

RV: down

FVC: down

FEV1: down

FEV1/FVC: up

lung compliance: down

lung resistance: down

raise dimension of thorasic cavity

active inspiration, primary muscle

innervated by phrenic nerve C3, C4, C5

barrels out lower ribs

active inspiration, secondary role

raise sternum and top 2 ribs

forced inspiration, accessory muscle

maintains airway flow, lowers resistance

forced inspiration, accessory

increase intra-abdominal pressure, pushes diaphragm up

forced expiration

flattens thorax, pulls ribs down and in,

forced expiration

elastin: stretch lung tissue

collagen: resist stretch

lung expand/stretch in inspiration b/c unfol + rearange fibers

recoil is reciprical to compliance

smokeing decreases recoil

Laminar flow

Turbulent flow

transitional flow

laminar flow: smooth in branches.  lung & small airways

Turbulent flow: trachea, high velocity

Transitional Flow: mix of both.  bronchial tree.

lung is most complient at FRC (40% of TLC)

lung becomes less complient as TLC is approached.  at high volumes, a big change in P is needed to raise V.

compliance increases with age

decreases with fibrosis, and alveolar edema

DPPC produced by type II granular pneumocytes

also contributes to compliance

Zone 1

Zone 2

Zone 3

Zone 1: P_A > P_a > P_v.  ventilated, but not perfused. (dead space)

Zone 2: P_a > P_A > P_v.  Blood flow is based on the difference between arterial pressure and alveolar pressure.  as the difference increases near the bottom of zone 2, pulmonary bloodflow will increase.

Zone 3: P_a > P_v > P_A.  bloodflow is dependent on difference between arterial and venous pressure.  capilarys are perminantly open.  vessels increase size on bottom of zone 3.  low resistance, high flow.

zone 1 can be increased if blood pressure drops from hemmorhage.

Nucleus tractuc solitarius

(NTS)

• in brainstem
• DRG ventrolaterally
• peripheral chemoreceptors & pulmonary stretch receptors: lateral
• arterial baroreceptors: dorsolateral & medial

• vagus nerve to lateral NTS
• smooth muscle of lungs
• activated by inspiration stretch
• when fully stretched, fires NT to medulla to stop.  "Breuer-Hering reflex"
• active during large V_T

• Vagus -> lateral NTS
• between airway epithelial cells
• when iritated: bronchoconstriction, rapid shalow breathing. 
• cough/sneeze

Type 1 alveolar cell

type 2 alveolar

1: gas exchange

2. surfactant

relaxes

dilation

FEF 25-75%

if small?

forced expiration: fast then slows down

forced inspiration: flow is constant

low FEF 25-75

low FEV1

high resistance

alveolar ventilation

(simple)

forced expiratory volume

if big?

if small?

whats normal?

FEV1

big: restrictive

small: obstruction if less than 0.6

norm: 0.8

40% of TLC

most complient

when little alvioli send air to big alvioli

not happen because

tension in parger alvioli increase

tension in small alvioli decrease

at FRC

FRC is resting, lung wants to adjust volume to reach FRC

Po₂ = P_b X Fo₂

Fo₂ = fractional component of o₂

PAo₂

atmospheric PAo₂

alveolar: 100 mm hg

atmospheric: 160

cell Po₂

Cell Pco₂

Po₂ = 40

Pco₂ = 46

pulmonary edema

pulmonary fibrosis

pneumonia

% oxygen saturation of hemoglobin.  % of Hb that have O₂

So₂ = amount of O₂ boung to Hb / O₂ capacity

curve shifted right

less Hb-O₂ affinity

CO poisoning

what happens to

O₂ content?

O₂ capacity?

O₂ content low

O₂ capacity same

for lung cell oxygen consumption

from aorta -> lungs -> azygous/intercostal vains -> right atrium

ACH

bronchoconstriction

Histamine: constriction by binding H1

Leukotriene: constrict, increase prosteglandins

forced inspiration

pulls lower ribs up and foarward

forced expiration

raise intraabdominal pressure

pushes diap[hragm up

forced expiration

flatten thorax

pressure in breathing during inspiration

intrapulmonary

intrapleural

intrapulmonary: (lung) down up

intrapleural: (outside) down

C_x = a X P_x

C_x = amount of gas disolved in liquid

a = solubility in the liquid

P_x = partial pressure of gas

Big Hb-O2 affinity

left shift

• Low 2,3 BPG
• High PH
• Cold
• ow Pco₂

• High 2,3 BPG
• Hot
• Low PH
• High Pco₂

O₂ content = (1.34 X Hb concentration X So₂) + (o.oo3 X Po₂

)

Hypoxic Hypoxia

what?

wht?

blood has loq Po₂

and Hb poorly saturated

why: hypoventilation, high altitudes, low Pio₂

anemic hypoxia

what?

why?

Po₂ is normal, Hb concentration is low

low O₂ content, and low O₂ capacity

why: carbon monoxide,

Hypoperfusion hypoxia

what?

why?

Circulatory/ischemia/stagnant hypoxia

What: low tissue bloodflow

Why: low CO, local obstruction

Histotoxic hypoxia

what:

why:

what: toxic substance inhibits ability to use O₂

O₂ content of venous blood high, O₂ consumption by tissue low.

why: cyanide

deoxygenated, reduced HbH will bind CO₂

if PO₂ is low, CO₂ will be high

bronchial circulation + pulmonary circulation

blood mixing, so blood to LA isnt 100% oxygenated.

PA > Pa > Pv

ventilated, not perfused

can increase if hemorhage low BP (hypovolemia),

Pa > PA > Pv

bloodflow dependent on Pa - PA

Pa > Pv >PA

bloodflow dependent on Pa - Pv

low resistance, high flow

poor get poorer

rich get richer

(from an O₂ perspective)