Physiology- Pulmonary System

what is required for aerobic respiration?

oxygen

aerobic respiration

• chemical process in which oxygen is used to make energy (ATP) from glucose

• waste products= CO2 and H20

function of pulmonary system

facilitate exchange of gases btwn environmental air and blood

• breathe O2 IN

  • cells use oxidative phosphorylation to make ATP (cellular/aerobic metabolism

• breathe CO2 OUT

  • CO2 is byproduct of cellular metabolism

  • needs to get out bc directly affects pH

pH

• measure of concentration of free hydrogen ions

  • lower pH= MORE H+=more acidic (acidosis)

  • higher pH= less H+= more basic (alkylosis)

how does CO2 cause acidosis?

• CO2 acts as a weak acid with H2O; carbonic acid can donate H+→ bicarbonnate and H+=acid

• CO2 + H2O ←→ H2CO3 (carbonic acid)←→ HCO3- + H+

pH=…

pH= 1/[H+]

pH= [HCO3-]/ [CO2]

• concentration of base/concentration of acid

pulmonary flow

1) fresh oxygen-rich air is brought into lungs and travels to the heart via pulmonary VEINS

2) left side of the heart pumps O-rich blood to the body via ARTERIES

3) skeletal muscle uses O2 to create energy and produces CO2 as waste

4) O2-poor and CO2 rich blood enters right side of heart and is pumped to the lungs via pulmonary ARTERIES

5) pulmonary arteries release CO2 into airway for expulsion into environment

structure of respiratory system

1) conducting airways leading to the lungs; nO GAS EXCHANGE

• nasal passages

• pharynx

• larynx

• trachea

• bronchi

• bronchioles

2) Respiratory zone: GAS EXCHANGE

• alveoli

3) respiratory muscles of chest and abdomen

components of pulmonary tree

1) conducting zone: conduct, clean, warm, filter, and humidify air

• dead space: no gas exchange

2) respiratory zone: alveoli and some terminal bronchioles

• pulmonary tissue interfaces pulmonary capillaries where gas exchange occurs

• surface area increases→ easier diffusion

alveoli

• specialized structures with very THIN walls (simple squamous epithelial) and very high surface area for the job of AIR EXCHANGE

• smooth muscle surrounds terminal bronchioles

concentration of blood from pulmonary ARTERY

• deoxygenated (high CO2 and low O2)

• going to ALVEOLI to become oxygenated

concentration of blood from pulmonary vein

• oxygenated (high O2 and low CO2)

• leaving alveoli→ heart to be pumped to tissues

steps to accomplish air exchange

1) ventilation

• exchange of gases btwn lungs and environment by MECHANICAL act of breathing

2) diffusion

• mvmt of air btwn lungs and pulmonary capillaries

  • O2 diffuses down concentration gradient

3) perfusion

• maintaining adequate blood supply to pulmonary capillaries

ventilation

mechanical mvmt of air or gas into and out of the lungs

minute ventilation

volume of gas inhaled or exhaled per minute

minute ventilation (L/min)= respiratory rate (RR) x tidal volume

respiratory rate

how frequnely inhale/exhale, measured in breaths per minute

“how many”

tidal volume

volume of air per breath

“how much”

alveolar ventilation rate (AVR)

RR X (TV-dead space)

• volume of air moving in and out of the alveoli that is actively participating in gas exchange

  • how much is available for gas exchange

• usually same as MV

primary ways to affect ventilation

1) affecting the RATE and DEPTH of breathing

• depth increases TV

2) affecting size/diameter of airway

• larger airway= < resistance, therefore more air comes through

both are under control of autonomic NS

chemoreceptors

signal respiratory center int he brain to increase or decrease RATE and DEPTH of breathing

central chemoreceptors

• located in the BRAINSTEM

• sense pH of CSF

peripheral chemoreceptors

• locate din the AORTIC ARCH and CAROTID BODIES

• sense CO2 and O2

  • primarily Oq in the blood

  • ex. detect hypoxia→ signal brain to increase resp rate and depth

what happens when a central chemoreceptor detects a pH of 7.29 on the CSF

the ventilatory rate and depth INCREASE

what happens when a peripheral chemoreceptor detects low levels of oxygen in the blood?

ventilatory rate adn depth will increase

how/why are signals sent to respiratory muscles from ANS?

via EFFERENT nerves to adjust ventilation to maintain homeostasis

effect of airway resistance on ventilation

• resistance to air flow has a DIRECT effect on ventilation

• resistance is determined by the diameter of the conducting airways (inverse)

• larger diameter= less resistence= easier to ventilate

• smaller diameter= more resistance= harder to ventilate

major site of airway resistance…

bronchi

• bronchioles are surrounded by smooth muscle to allow for vasoconstriction/dilations

bronchodilation/constriction with Sympathetic nervous system

• when sympathetic nervous system (fight or flight) is activated→ bronchodilation

• epinephrine NT binds to BETA-2 receptors that cause dilation→ increase in air

bronchodilation/constriction with Parasympathetic nervous system

• resting, therefore don’t need as much air

• acetylcholine binds to MUSCARINIC receptors to constrict brochioles

• ex. antimuscasrinic helps with asthma to dilate

key factors that influence breathing mechanics

changes in pressure

1) respiratory muscle use

2) pleural fluid and intrapleural pressure

3) elasticity and compliance of the lungs

4) airway resistance

function of respiratory muscles

• intercostals and diaphragm expand or contract to manipulate the volume of the intrathoracic space

• INHALATION: diaphragm contracts (move down) and ribcage expands as rib muscles contract

  • increase volume and decrease pressure

• EXHALATION: diaphragm releases (moves up) and rib cage gets smaller as rib muscles relax

  • decrease volume and increase pressure

boyle’s law

1) increasing VOLUME will decrease the pressure in the container

2) air will move from area of high pressure to low pressure

• diffusion down concentration gradient

utilizing pressure gradients

• intrapulmonary pressure during INHALATION= atmospheric pressure of -1

  • increased volume and decreased pressure inside the lungs (lower than atmospheric) therefore O2 travels down concentration gradient and into lungs

• intrapulmonary pressure during EXHALATION= atmospheric pressure +1

  • decrease volume and increase pressure; drives O2 and gas out

muscles of inhalation

• active process therefore muscles must be activated to perform inhalation

• PRIMARY muscles: diaphragm and external intercostal

• ACCESSORY muscles: abdominal muscles, anterior scalene, sternocleidomastoid

  • greatly used in instances of respiratory distress

elasticity and compliance

ELASTICITY

• tendency of tissue to return to its OG change and volume

• greater elasticity= greater recoil

• lungs coming back “in”

COMPLIANCE

• change in volume that occurs per unit change in pressure OR the ease with which an elastic structure stretches in response to pressure

• lungs going “out”

more elasticity= less compliance

elastic recoil

• acts as a force causing lungs to move INWARD

• allow EXHALATION to be PASSIVE process under normal conditions

  • do not need to engage muscles due to natural elasticity

compliance

• compliance of lungs and chest wall allows expansion OUTWARD resulting in ability to appropriately inspire

factors that combat lung compliance

1) elasticity of the lungs

2) surface tension of alveoli

forces act to pull lung tissue INWARD

• increase in either will lead to a decrease in lung compliance/more difficult to inhale

surface tension in the airway

greater the surface tension in the airway, the more collapsed tje alveoli (less compliance)

importance of surfactant

• alveoli have a thin layer of fluid/water to protect thin epithelial cells (TYPE 1 ALVEOLAR CELLS) from irritants

• fluid creates surface tension

  • water wants to stick together, therefore pulling inward on the alveolous→ wants to collapse

• surfactant: lipoprotein produced by TYPE 2 ALVEOLAR CELLS

  • inserts itself btwn water molecules to reduce surface tension→ makes alveoli more compliant and able to expand

clinical relevance: pulmonary fibrosis

• lungs become scarred→ inhibit compliance, therefore cannot expand and cannot bring in air→ hypoxia

clinical relevance: emphysema

• elastin is damaged therefore airway is schronically stretched/enlarged, therefor cannot breathe out→ increased CO2

• obstructive disease

pleural space

• maintain negative pressure relative to the lungs to prevent lungs collapsing inward

• contains pleural fluid

  • lubricant to prevent friction btwn lungs and chest wall with mvmt of inhalation dn exhalation

how is the intrapleural space (or pressure within pleural space) maintained negative relative to the intrapulmonary pressure?

1) elastic recoil of lungs (IN)

2) surface tension of the alveoli (IN)

3) chest wall elasticity (OUT)

Airway resistance

• resistance to airflow is increased with a decrease in airway diameter

  • bronchoconstriction

    • ex. asthma: smooth muscle around bronchioles with tighten and constrict airway causing increased reistance

  • inflammation

    • ex. bronchitis or pneumonia: infected airway becomes inflamed→ decreased airway diameter

  • obstruction

    • ex. swallow foreign body

spirometry

• pulmonary function test that tests ventilation ONLY

• measure VOLUME and FLOW of air inhaled adn exhaled against time

• useful in diagnosing different type of pulmonary diseases

  • restrictive vs obstructive

aspects of spirometry

• tidal volume

• vital capacity

• residual volume

tidal volume

volume of air moving in or out with each NORMAL breath

vital capacity

MAXIMUM tidal volume with DEEPEST inhale and exhale

residual volume

the amoutn of air REMAINING IN THE ALVEOLI after max exhalation

• keeps alveoli from complete collapse

flow volume looops

• traces velocity of air mvmt and volume of lungs through max inhalation adn exhalation

• changes in VELOCITY can indicate INCREASED airway resistance or elastic recoil

  • slows air mvmt (in or out)

• changes in VOLUME can indicate DECREASED compliance, elastic recoil, or increased airway resistance

  • cannot fully inhale or exhale

why is the airway a potential route of infection for pathogens?

it is in constant contact with external environment

irritant receptors

• epithelium of conducting airways

• sensitive to noxious (pollen, dust, bacteria, etc)→ stimulate cough

cough reflex

• protective reflex that helps clear airways by explosive exhalation—closing off; decreasing volume and increase pressure→ open and expel irritant

  • inhalation

  • closure of glottis

  • exhalation muscle contraction

    • abdominal muscles

  • opening of glottis→ expel irritant

• can be stimulated by higher brian (voluntary( or reflex pulmonary irritant stimulation

what is the goal of the mucociliary escalator?

protect the sensitive thin-walled tissue of the alveoli that are vital fro gas exchange

muscociliary escalator

• epithelial lining of bronchi contains:

  • goblet cells and mucus glands

    • goblet cells: trap irritants/pathogens

    • cilia:hairlike projections that move mucus
      up and out”

alveoli defenses

1) alveolar macrophages

• highly prevalent

• engulf pathogens

• initiate adaptive immune response

• stimulate inflammation

2) surfactant

• bacteriostatic properties

  • limit bacterial growth/proliferation

perfusion

bring blood to lungs and out to the body

diffusion

mvmt of molecules (CO2 and O2) across alveolar membrane

process of diffusion

1) O2 will diffuse DOWN it’s concentration gradient from the alveoli to the vasculature (PULM VEIN)

2) CO2 will diffuse down it’s concentration gradient form the vasculature into the alveoli (from PULM ARTERY)

respiratory membrane

*where gas exchange via diffusion occurs

• site of EXTERNAL RESPIRATION

• contains:

  • type 1 alveolar cells

  • thin connective tissue

  • capillary wall

• diffusion is optimized due to small area

external respiration

mvmt of O2 and CO2 across the respiratory membrane

• O2: moves into cap

  • inhaled air as high PO2

  • deoxygenated blood in pulm ARTERIAL capillaries have LOW PO2

• CO2: moves into alveoli

  • deoxygenated blood in pulm ARTERIAL capillaries have HIGH CO2

  • inhaled air has LOW CO2

partial pressure of oxygen (PO2) in blood from heart and system circ

low; 40mmHg

partial pressure of oxygen (PO2) from fresh air

high; 100mmHg

pressure gradient for oxygen btwn alveolar air and deoxygenated blood is …..

~60mmHg

what factors impact the process of diffusion?

1) surface area of membrane

2) MAGNITUDE of partial pressure gradient

• larger=increase drive of diffusion

3) thickness of semi-permeable membrane

4) solubility of gas (CONSTANT)

• O2 and CO2 must move through thin layer of alveolar fluid, interstitial fldid, and plasma

• CO2 is 20x more soluble than O2

  • lower magnitude of change due to higher solubility

why administer oxygen therapy to patients with hypoxia?

to manipulate the pressure gradient at the alveolocapillary membrane

• improved diffusion due to increased magnitude

internal respiration

mvmt of O2 and CO2 btwn TISSUES and systemic capillaries

• CO2: CO2 moves out of tissues into blood (VEINS)

  • systemic arterial cap have low CO2

  • tissue cells have HIGH CO2

• oxygen: O2 moves into cells of tissue (from arteries)

  • systemic arterial cap have HIGH PO2

  • tissue cells have low PO2
    

oxygen-hemoglobin dissociation curve

heme affinity for oxygen changes depending on environment:

1) O2 rich-> heme binds O2 more readily

2) O2 poor→ heme releases O2 more readily

O2 rich environment (high PO2)

• heme grabs and HOLDS on to as much O2 as possible when available and tissues are not demanding

why does heme bind/release oxygens based on environemnt?

cooperative/allosteric binding

• when O2 binds one subunit→ conformational change in adjacent peptide subunits to make them have HIGHER affinity for O2 binding → adjacent subunit changes shape and now binds O2 with higher sffinity, etc

O2 poor environment (low PO2)

hemem readily gives up O2 to the tissue that need it

• decrease in cooperative binding due to low conc of O2

why does increase in CO2 decrease affinity for O2

CO2 as a product→ decreased Ph (more acidic)→ decrease affinity for O2

• right shift

factors that cause LEFT shift in heme-O2 curve

INCREASED afffinity for O2

1) decr. pCO2

2) decr. [H+]

3) decr temp

4) HbF

factors that cause RIGHT shift in heme-O2 curve

DECREASED affinity for O2

1) incr pCO2

2) incr [H+]\incr temp

pH effect on heme conformation

• H rich environments (low pH) heme molecules will bidn O2 with LOWER affinity

  • metabolically active tissues (which prod more CO2), heme is more likely to drop off O2 and deliver to tissue

PaO2

actual O2 content in arterial blood

• only small amnt and invasive procedure that only gives quick snapshot

O2 saturation (SPO2)

• percent o fheme binding to sites in blood that are carrying O2

  • cons: if decreased heme (anemic), O2 carryign capacity is cut, therefor all heme will try to adhere to more O2→ false high saturation

relationship btwn PaO2 and O2 sat

• PaO2 of 70-90 is normal

  • correlates with O2 sat ~90%

• direct correlation: incr PaO2=incr O2

what influences perfusion?

1) CARDIAC OUTPUT

• vol of blood pumped by heart per minute

  • R ventricle feeds pulmonary ARTERY circulation

2) pulmonary vessel diameter

• pulm vasoconstriction/dialtion

  • dilation: INCR perfusion

  • constriction: DECR in perfusion

what major process can be manipulated by the body for appropriate oxygenation

ventilation and perfusion

ventilation-perfusion matching

• vent and perf both require energy adn effort

• waste of energy to vent area with poor perf and vice versa

• goal= MATCH vent and perf

  • avoid wasting energy and maximize gas exchange

matching vent and perf

ratio of Vent/perf shoud be ~1

V-how much air into lung

Q- how much blood into air space

V/Q=1

vent and perf ratio

• flow of O2 into alveoli (vent) is almost equal to the flow of deoxygenated blood ip the alveolar cap

vent and perf mismatch

1) area receiving O2 well (vent well) but the blood flow through the capillary is decreased (not perf well)— V/Q>1

• ex. PE→ not enough vent

2) areas receiving adequate blood flow (perfusing well) but isnt bringing enough O2 to the alveoli (vent poorly)- V/Q<1

matching V/Q: increased AVR

• increased AVR (V=6L.min)

  • V/Q=6/5=1.2

  • wasted air mvmt

• how keep matched?

  • Incr AVR=incr PpO2

    • O2 diffusing across resp membrane stimulates N2O prod by capillaruy endothelial cell

    • N2O causes smooth muscle to RELAX→ vasoDIALITON→ incr perfusion

matching V/Q: hypoxic pulm vasoconstriciton

• poorly ventilated alveolus

  • V/Q=3/5=0.6

  • wasted perfusion

• how keep matched?

  • decr AVR=decr PO2

  • decreased O2 diffusing across resp membrane suppresses N2O prod

    • absence of N2) causes smootj musclecontraction/CONSTRICTION

    • decrease perf

pulm adaptations: acid-base balance

• immediate responder to acid/base disorders to regulate pH

• pH=[HCO3-]/[CO2]

pt is in respiratory failure and cannot properly exhale CO2 rich air into the environment. WHat is the effect on pH?

• decrease/become more acidic

  • RESPIRATORY ACIDOSIS

pt hyperventilating and expiring immense amnts of CO2 into atmosphere. What is the effect on pH?

increase pH/more basic

• RESPIRATORY ALKALOSIS

pt is in renal failure and cannot properly re-absorb HCO3- effectively in the kidneys? what is the effect on pH?

decrease in pH/more acidic

• METABOLIC ACIDOSIS

pulm response to acidosis

• acidosis = LOW pH

• how fix?—incr CO2 exhalation

  • chemoreceptors (brainstem and aorta/carpotsi) detect low pH

  • resp center of brainstem proccesses afferent signals, triggers:

    • INCR depth o ventilation

    • INCR resp rate

pulm response to alkalosis

• alkalosis= HIGH pH

• how do we fix? incr CO2

  • chemoreceptors detect high pH

  • proccess afferent signals, triggers

    • decr depth of vent

    • der resp rate