physio exam 3

how is the respiratory system analogous to the CV?

• pump rate

• fluid and flow rate

• site of regulation of R

• exchange surface

how long can brain cells survive without o2?

4-6 min

path of air

nasal cavity

pharynx

larynx

trachea

bronchi

bronchioles

conducting zone of path of air

trachea

bronchi

bronchioles

terminal bronchioles

respiratory zone

respiratory bronchioles

alveolar ducts

alveolar sacs

path of gas exchange

ventilation

gas exchange

CV: heart pumps blood

gas transport in blood to cells

what is the driving force of air flow?

pressure gradient

intra-alveolar pressure must be lower than outside for air to move in

regulation of conducting airways

autonomic

what muscles are used in active inspiration?

SCM

scalenes

external intercostals

what muscles are used in active expiration?

abdominals

internal intercostals

how does inspiration effect lung volume and pressure?

volume increases, pressure decreases

how does expiration effect lung volume and pressure?

decrease volume, increase pressure

quiet inspiration

pacemakers of RCC fire

signal somatic motor neurons to fire

diaphragm, external intercostals, scalenes contract

volume increases, pressure decreases

air moves in

equilibration with atm pressure

What is the efferent in the respiration

pathway?

Somatic motor neurons

Which is NOT true of

quiet expiration?

A. The diaphragm and external intercostals relax

B. Intra-alveolar pressure becomes greater than

atmospheric

C. The internal intercostals and abdominals contract

D. The elastic aspects of the lung recoil

C. The internal intercostals and abdominals contract

Transpulmonary pressure (TPP) gradient

intra-alveolar – intrapleural

How does the pulmonary pressures graph change

with forced respiration?

intra pleural pressure is lower at the end of inspiration

What happens when transpulmonary pressure =

zero?

lung collapses

pneumothorax

• air in pleural space

• due to external puncture or internal rupture

two major factors of work of breathing

lung compliance

airway resistsance

what is lung compliance

• tissue integrity

• surface tension/surfactant

• Inversely related to the elastic properties of

  lungs

elastance

•The ability of the lungs to return to their

original shape

•AKA elastic properties/recoil

•Related to the amount of Collagen and Elastin

in connective tissue (elastic tissue)

emphysema

• low elastance

• high compliance

• stretched out like a rubber band

• difficult for air to leave lungs, air stays trapped in lungs

components of alveoli

• type I cells for gas exchange

• type II cells to synthesize surfactant

• capillaries

• elastic fibers

• macrophage

fibrosis

• increased elastance

• lowered compliance

• increased scar tissue/collagen

• difficult to expand and fill lungs

surface tension on alveolus

• hydrogen bonding between h20 molecules

• exerts inward pressure

• makes alveoli difficult to expand

law of laplace

• inward/collapsing pressure described by law of la place

• P=2T/r

• P= inward pressure

• T= surface tension

• r= radius of alveolus

Smaller alveoli . . .

A. Have greater inward-directed pressure than large

alveoli

B. Have less inward-directed pressure than large

alveoli

C. Have same pressure as large alveoli

Have greater inward-directed pressure than large

alveoli

small alveoli

• good for gas exchnage bc of high surface area

• high collapsing pressure

• surfactant solves this problem

surfactant

breaks up Hbonding and surface tension

decreases collapsing pressure in small alveoli

• 80% phospholipid

(dipalmitoylphosphatidyl choline or DPPC)

• Secreted by type II cells

• Forms interface between water and air in alveolar

lumens ….decreases and equalizes surface tension

• increases compliance

surfactant disorders

• neonatal respirstory distress syndrome

• acute respiratory distress syndrome

neonatal respirstory distress syndrome (NRDS)

• premature and no surfactant production

• small alveoli collapse

• no gas exchange

• hypoxemia (low O2 in blood)

acute respiratory distress syndrome (ARDS)

• inflammatory process

• reduced surfactant synthesis, increases surfactant breakdown

• no gas exchange

• hypoxemia (low O2 in blood)

causes of ARDS

• coronavirus & SARS

• sepsis

• blood transfusions

• a serious head or chest injury

• smoke inhalation

• near drowning

• drug overdose

• pancreatitis

• shock from any cause

bronchoconstriction

parasympathetic

hystamine and leukotrienes

bronchodilate

sympathetic

CO2

airway resistance disorders

asthma

bronchitis

emphysema

tissue integrity disorders

emphysema

fibrosis

restrictive diseases (low compliance)

fibrosis

NRDS

ARDS

COPD

bronchits and emphysema

COPD triad

bronchitis

emphysema

asthma

Choose all true re: work of breathing:

A. Compliance and elastance are inversely related

B. Emphysema is the only high compliance

disorder

C. Fibrosis, ARDS, NRDS obstruct air into lung

D. High elastance = great ability to stretch

E. None true

A. Compliance and elastance are inversely related

B. Emphysema is the only high compliance

disorder

the resulting increase in interstitial fluid in the lungs is known as

pulmonary edema

what is the effect on diffusion of gases from alveoli into

capillaries?

rate of diffusion decreases because diffusion diststance increases

If the fluid enters the alveoli, what is the effect on surface

tension and recoil?

both increased

What happens if the inward-directed pressure of surface tension

is greater than the outward-directed transpulmonary pressure

gradient?

lung collapse

how are most lung volumes measured?

spirometry

what lung volume can’t be measured through spirometry?

residual volume

Tidal Volume

Quiet Breathing

(quiet inspiration and expiration)

Inspiratory Reserve Volume (IRV)

Forced Inspiration

Expiratory Reserve Volume (ERV)

Forced Expiration

residual volume

Amount of air that remains within

lungs after a forced exhalation that

participates in gas exchange

• Most of this residual volume exists

  because the lungs are held stretched

  against the ribs by the pleural fluid.

functional residual capacity

volume remaining in the lungs after a normal tidal volume is expired and

can be thought of as the equilibrium volume of the lungs

Equilibrium volume:

inward elastic recoil force of the lungs = outward force of the

thoracic wall (no exertion by the diaphragm or other respiratory muscles)

Vital capacity

max volume someone can exhale from forced inspiration.

Increases with body size and physical conditioning; decreases with age

dead space

- the volume of the airways and lungs that does not

participate in gas exchange.

- anatomical dead space (conducting airways) + physiologic

dead space (alveoli that are not perfused or poorly perfused)

- The dead space to tidal volume ratio in healthy lungs is

constant at about 0.3

volume of fresh air entering the alveoli

tidal volume minus the dead space volume

How do we measure efficiency of breathing?

Total pulmonary ventilation (TPV)

Alveolar ventilation

TPV

ventilation rate (breaths/min) x tidal volume (VT)

Alveolar ventilation

ventilation rate (breaths/min) x (tidal volume – dead space)

characteristics of asthma

mucus

inflammation

broncoconstriction

characteristics of bronchitis

mucus

inflammation

characteristics of emphysema

bronchiolar collapes

How are obstructiv disorders diagnosed?

FEV1 pulmonary function: Volume of forced vital capacity expired in 1 second

obstructive disease FEV1/FVC

decreased

restrictive disease FEV1/FVC

FEV1/FVC increased

Ventilation-perfusion (V/Q) matching

coordination between the amount of air (ventilation) reaching the alveoli and the amount of blood (perfusion) flowing

for successful gas exchange

ATM O2 determines…

Alveolar O2 determines…

Plasma O2 determines…

HbO2

affects ATM O2

altitude

humidity

affects alveolar O2

lung compliance, airway resistance

affects plasma O2

factors affecting diffusion

local control

optimize gas exchange

which type of arteriole constricts in the presence of low O2?

pulomonary (conserve profusion)

what do pulmonary arterioles do in hypoxia?

constrict

what do pulmonary arterioles do in hyperoxia?

dilate

low V/Q

• low ventilation

• perfusion wasted

• ex. COPD, pulmonary edema

high V/Q

• ventilation wasted

• low profusion

• ex. emphysema?

V/Q = 0

• ventilation = 0

• shunt

• ex. airway obstruction, pneumonia

V/Q = unlimited

dead space

• no profusion

• pulmonary embolism

path for successful gas exchange

1. O2 needs to reach alveoli (low V/Q)

2. O2 needs to diffuse across

3. O2 needs to reach blood (high V/Q)

what would cause a decrease in ventilation?

• airway obstruction

• obstructive lung disorder

• restictive lung disorder

what would can an increase in ventilation?

emphysema

what would cause a decrease in perfusion?

low cardiac output

pulmonary embolism

PO2 in emphysemsa

low

PO2 in fibrosis

low

• decreased ventilation

• thick walls, decreased gas exchange

PO2 in pulmonary edema

• fluid in interstitial space increases diffusion distance

• PO2 low

PO2 in asthma

increased airway resistance

bronchioles constricted

• PO2 low

what happens when PCO2 increases?

bronchioles - dilate

pulmonary arterioles - constrict

systemic arterioles - dilate

what happens when PCO2 decreases?

bronchioles - constrict

pulmonary arterioles - dilate

systemic arterioles - constrict

what happens when PO2 increases?

bronchioles - constrict

pulmonary arterioles - dilate

systemic arterioles - constrict

what happens when PO2 decreases?

bronchioles - dilate

pulmonary arterioles - constrict

systemic arterioles - dilate

if V/Q < 0.8, what happens to plasma gas

content?

O2 decreases, CO2 increases

total blood O2

• <2% PO2 (dissolved in plasma)

• 98% HbO2 (bound to hemoglobin)

Why does our body use O2 bound to hemoglobin

and not dissolved O2?

Oxygen is not very soluble in liquid

hemoglobin

• each heme group hasa. prophyrin ring with an iron atom in the center

• in most adult hemoglobin, there are two alpha chains and two beta chains

• one hemoglobin can bind up to four oxygen molecules

cooperative binding

More O2 binds to Hb,

increases affinity of Hb

to O2

Cooperative binding is biologically

advantageous

Why?

1. Hemoglobin is at 75% saturation when it

returns to the lungs, possessing the

highest affinity to O2 – perfect for O2

binding to Hgb at the lungs

2. When there is less O2 bound, Hgb’s

affinity to O2 decreases, so more O2 will

unbind. This is perfect for when you need

to offload O2 quickly (think running away

from tigers)

How do you unload O2?

Decrease Hb affinity to O2

When do you need to change the affinity to O2 aka unload more O2?

Running away from tigers aka increased metabolic state in which you are

using up lots of O2

What normal factors can change the affinity of Hb?

Metabolic byproducts:

- CO2 (a byproduct of cellular respiration)

- pH (H+ is a byproduct of CO2 breakdown)

- Temperature (a byproduct of muscle movement)

- 2,3 BPG (a byproduct of metabolism)