KIN 3515 EXAM 3 Pulmonary

pulmonary system

pulmonary system functions

02 delivery, CO2 removal, acid-base balance blood pH

facilitate speech and sound, defend against microbes

particle filtration, traps and dissolve blood clots

add or remove chemicals

ventilation

mechanical drawing in and expelling of air via breathing

gas exchange between atompshere and air sacs (alveoli) in lungs

pulmonary ventilation

process of ambient air moving in and exchanging w air in lungs

lungs provide gas exchange surface separating blood from gaseous environment

humorous bifurcations and infolding by point air reaches the alv

lungs into blood

O2 move from

blood into lungs

CO2 move from

respiration

sum of all physiological processes that accomplish passive moving of 02 from atmosphere to tissue in support of cell metabolism and continual passive movement of CO2 form tissues in atmosphere

external respiration

exchange of O2 and Co2 between external environment and cells

cellular respiration

intracellular metabolic processes carry out in mitochondrial which uses O2 and produce CO2 to generate energy from nutrients

conductive zone

air enter via nose and mouth

air is body temperature, filtered by mucus, humidified

trachea → bronchi

bronchioles→ smaller terminal bronchioles

transitional zone

branching of bronchioles get smaller and smaller as air move from conduction zone

very small amount of gas exchange can occur

respiratory bronchioles → alveolar ducts

respiratory zone

branching increases in transitional zone

where MOST gas exchange occur, alveolar sacs

alveolar sacs

elastic thin walled (1 cell layer) membraneous sacs, lined by surfactant

vital surface for gas exchange between lung tissue and blood

largest blood supply of organ and all of it

alveoli and capillaries

millions of short thin walled blank and blank that lie side by side

surfaces thin as possible w compromising structure

capillary blood

gas diffuse across extremely thin barrier of alveolar and capillary cells

O2 cross alveolar air into ?

alveolar air

gas diffuse across extremely thin barrier of alveolar and capillary cells

CO2 cross capillary blood into?

boyles law

volume decrease, pressure increase

inverse volume increase, pressure decrease

changes in volume in chest cavity during ventilation create pressure gradients that drive air flow (atmosphere 760 mmHg)

air flow into lungs

chest volume decease, alveolar pressure fall (759)

air flow ?

air flow out of lungs

chest volume decrease, alveolar pressure (761)

aire flow?

inspiration

diaphragm contract, flatten, move into abdominal space

contraction of scaleni and external intercostal muscles rotate and lift ribs ups + away from body

elongation and enlargement of chest cavities expand air of lungs causing intra-alveolar pressure to decrease below atmospheric

air sucked through nose and mouth filling and inflating lungs

ends when thoracic cavity expansion cause intra-alveolar pressure to equal atmospheric

expiration

results from natural recoil of stretched lungs tissue and relation of inspiratory muscles

chest cavity volume decreased and alveolar gas compress causing air to move out respiratory zone into atmosphere

during strenuous exercise utilize internal intercostals and abdominal muscles

ends when compressive force at expiratory muscles ends and intra-alveolar pressure decrease to back atmospheric

surfactant

lipoprotein mixture produced by alveolar epithelial cells

reduced alveolar membrane surface tension which reduce energy requirement for alveolar inflation

makes breathing easier

surface tension

force exerted by water molecules on surface of alveoli as water molecules pull together

as water moles pull together form small surface area to interact w air in lungs it pulls the alveoli closed

greater surface tension surrounding alveoli greater the force require to overcome pressure in sphere and enable to inflate

measuring lung volume

spirometer used to measure static lung volume

tidal volume TV

volume of inspired or expired air per breath

0\.4-1L @ rest

depth of breathing

inspiratory reserve volume IRV

max volume can INSPIRE over and above resting tidal volume

2\.5-3L

expiratory reserve volume ERV

max volume can EXPIRE over and resting TV

1-1.5 L

residual lung volume RLV

volume remaining in lungs after max expiration

0\.8-1.2L

inspiratory capacity IC

max volume of air inspired, 3-4 L

TV + IRV

functional residual capacity FRC

volume remaining in lungs after tidal expiration, 2-2.2L

ERV + RLV

forced vital capacity FVC

max volume of air EXPIRED after max inspiration, 4-5L

TV+ IRV+ ERV

total lung capacity TLC

max volume of air lungs can hold, 4-7L

TV + IRV + ERV+ RLV

dynamic ventilation

depend on max forced vital capacity breathing rate

air flow velocity

depend on resistance of passages to smooth flow of air turbulence and lung compliance/elasticity

forced expiratory volume FEV

FEV1.0, volume of air expired over 1st second of EXPIRE

pulmonary airflow capacity PAC

reflect pulmonary EXPIRE power on driving pressure

FEV/ FVC

minute ventilation VE

volume of air moving past mouth and nose

VE equation

=TV x breathing rate

mL/breath x breaths/min

alveolar ventilation VA

volume of air reaching alveoli each min

VA equation

=breathing rate x (TV- anatomical dead space)

breaths/min x (mL/breath- mL/breath)

anatomic dead space

volume of air remaining in conduction zone, set of volume of air (30% of tidal volume)

increasing rate or of breathing increases VE

increasing depth of breathing increase VA

tidal volume rarely exceed 60% of FVC, come from reducing IRV and ERV

physiologic dead space

portion of alveolar volume w V:P ratio near ZERO

ratio of alveolar ventilation to pulmonary blood flow

no gas exchange occur due to under perfusion of blood or inadequate ventilation relative to alveolar space

CAN change in volume

@ rest, VA= 2.3L/min

5L blood flow thru pulmonary capillaries = 0.84

hyperventilation

increase in pulmonary ventilation exceed oxygen needs of metabolism, hypocapnia

hypocapnia

low blood CO2 and ALKALOSIS

hypoventilation

reduced pulmonary ventilation, hypercapnia

hypercapnia

high blood CO2 and ACIDOSIS

apnea

transient cessation of breathing

hyperpnea

increased pulmonary ventilation due to exercise rate matches needs

dyspnea

shortness of breath, often assoc. w hypercapnia and acidosis

hypoxia

insufficient 02 @ cellular level

breathing

provide continuous fresh 02 for pickup by blood and Co2 removal from blood

blood

transport system between lungs and tissues

tissues

remove 02 from blood and put CO2 into blood

gas exchange

in lungs and tissues is PASSIVE process involving simple diffusion, NO ACTIVE transport (ATP requiring) mechanisms exist

PA02

partial pressure of 02 in alveolar chambers

Pa02

partial pressure of 01 in arterial blood, dissolved 02

Sa02%

percent saturation of 02 arterial blood with 02

Pv02

partial pressure of 02 in venous blood

PAC02

partial pressure of C02 in alveolar chambers

PaC02

partial pressure of CO2 in arterial blood, dissolved C02

PvC02

partial pressure of C02 in venous blood

Sv02%

percent saturation of venous blood with 02

a-v02 diff

arterial-venous oxygen differences

partial pressure PP

molecules of each specific gas in mixture of gases exert own pressure, depend on # of molecules of gas in volume, humidify and temperature, mmHg

PP

= % concentration x total pressure of gas mix

daltons law

mixture of total pressure sum of PP of individual gases in mixture

henrys law

oxygen and other gases diffuse from area of high pressure to low pressure

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rate of diffusion depend on

pressure differential between gas above fluid and gas within the fluid

quantity of gas dissolved

=solubility coefficient x (gas PP/ total barometric pressure BP)

(mL/dL)

solubility

dissolving power of gas determines # of moles moving in or out of fluid

mL of gas/ 100mL of fluid

coefficients for blood

C02 (57.03 mL)

02 (2.26 mL)

N2 (1.30 mL)

quantity dissolved equation

(mL gas/100mL fluid) = solubility coeff. x (PP/total BP)

ficks law

diffusion rate across membrane

directly proportional to tissue area, diffusion constant and pressure differential of gas on each side of membrane

inversely proportional to thickness os tissue

factors impacting diffusion rate

length of diffusion path, blood gas barrier \~2 cells thick

PP gradient, # of capillaries

\# of RBC-> hemoglobin concentration in each RBC

02

travel from high→ low pressure as dissolves and diffuses through alveolar membranes into the blood

C02

travel from high → low pressure as it move from blood to lungs

nitrogen

remain unchanged in gas exchange in lungs

alveolar gas

blood equilibrium occur in no more than 0.25 seconds

1/3rd RBC transmit time through lung capillary @ rest

@ rest blood leaving lungs \~100mmHg 02, 40mmHg C02

maintain slower blood flow velocity

with increasing exercise intensity, the blood volume in capillaries increases to..?

tissues

where 02 used fro energy metabolism and C02 produced

TCA Cycle → C02 produced

ETC → 02 used

@ rest in muscle P02= 40 mmHg and PC02=46mmHg

vig exercise P02=0mmHg and PC02 =90 mmHg

gas exchange in tusses

02 move from blood to muscle

C02 move from muscle to blood

blood move from arterial circuit into venous circuit as pass through tissue capillaries → a-v 02 difference

pressure gradient

blood dont lose all 02 and C02 as min level needed to drive ventilation and Acid-Bae balance

hemoglobin

iron protein molecule in RBC that bind 4 oxygen molecules

no enzymes require just appropriate PP

each Hb can carry 1.34 mL of 02, \~15g Hb/100mL blood

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oxyhemoglobin

normal Hb w iron reduced forming Fe++ (iron oxidized)

Fe++ share electrons and bonds with 02

in blood vessels that leave lungs and go toward body

deoxyhemoglobin

when oxyhemoglobin dissociate and release 02

iron still in Fe++ state

in blood vessels in peripherary and return to lungs

carbaminohemoglobin

normal Hb combined w C02 in blood vessels in periphery in return to lungs

carboxyhemoglobin

normal Hb combined w carbon monoxide C0

C0 bond w Hb, 210x stronger than bond with 02

transport 02 to impaired tissue

methemoglobin

iron oxidized (Fe++), cannot bind 02 in this state

tense state

subunits of Hb held together by electrostatic forces when deoxygenated

loading of 1 02 mole to 1 Hb binding site cause Iron mole and peptide attached to move slightly and interrupt electrostatic forces

hemoglobin cooperative binding

relaxed state

Hb looser and more readily bind 02 into 3 remaining binding sites

when 02 bound → oxyhemoglobin

oxygen transport cascade

changing PP as 02 pressure as 02 move from ambient air to mitochondria in active muscle tissue drive assoc. of 02 w HB

high PP

02 load onto Hb

low PP

02 unload from Hb

oxyhemoglobin dissociation curve

P02 determine amount of 02 carried by mechanism in blood

dissolved 02 → liner relationships btwn P02 and 02 content in blood

Hb02→ sigmoidal relationship btwn P02 + 02 content in blood based on cooperative binding

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concentration of Hb

important determinant of capacity of blood to hold 02

anemia, polycythemia

anemia

reduced Hb due to low iron stores

polycythemia

over production of Hb

bohr effect

any change in plasma acidity, PC02 or temperature shift oxyhemoglobin dissociation curve

more acidic and higher temp shift down and right, also indicate altered Hb molecular structure which reduce ability to hold 02, 20-50 mmHg P02 range

less acidic and lower temp shift up and down

maximizing 02 transport

4 influential factors for bohr effect

pH increased H++ ions, 7.4→ 7.35 shift

PC02, 40 mmHg to 43 mmHg

Temperatrue, luns 37 C muscles 38C

2,3 Diphosphoglycerate (DPG)

myoglobin and oxygen delivery

iron containing globular protein in skeletal and cardiac muscle providing intramuscular 02 storage, only store 1 mole of 02

higher affinity for 02 than Hb

affinity for 02 NOT influenced by pH, C02 or temperature

oxygen loading

retains 02 @ much lower P02

myoglobin and oxygen delivery