Week 10 & 11 - Respiratory System

Functions of respiratory system

1. Exchanges of gases (O2 & CO2) between atmosphere and blood

2. Maintain blood pH homeostasis (via CO2)

3. Protection from airborne pathogens

4. Vocalisation/speech

External respiration

4 parts

Ventilation: Exchange of air b/w atmosphere and lungs

• Inspiration/inhalation: Movement of air into the body

• Expiration/exhalation: Movement of air out of the body

1st Gaseous exchange: CO2 and O2 exchange at lung site

Gas transport: Movement of O2 and CO2 through the blood around the body

2nd Gaseous exchange: CO2 and O2 exchange at body tissue site

Segregation of respiratory system

Upper respiratory system: Anything above trachea

Lower respiratory system: Including trachea and anything below

Thoracic cavity

Where the lungs are, ribs on the side and diaphragm on the bottom.

Inside bordered by a pleural membrane cushion (2 sides) - contains ~ 25ml of pleural fluid

• Moist, slippery surface for when lungs move

• Holds the walls of the lungs open like a “suction”

  • Thus, lungs are usually partially open at all times

Cartilage in lower respiratory system

Cartilage: is in trachea to bronchi - conducting system

Smooth muscle: is mainly in bronchioles and alveoli - exchange surface

Alveoli structure

Wrapped with capillaries for gas exchange.

Wrapped with collagen & elastin for elastic recoil while breathing

Type 1 Alveolar cells - ~90% of cells in alveoli, where gas exchange occurs

Type 1 Alveolar cells/ surfactant cells - not used in gas exchange, keeps alveoli inflated

Alveolar macrophages - immune cells that eliminate pathogens

“Conditioning” air before it enters the lungs

1. Warming the air in the nasal cavity via ridges making turbulent flow

2. Making air 100% humid in the nasal cavity via ridges making turbulent flow

3. Filtering out foreign material (e.g dust)

Filtering out foreign material (e.g dust)

Occurs in the conducting zone (a.k.a trachea & bronchi) where there are ciliated epithelial cells. Goblet cells sandwiched b/w cilia produce mucus.

• Between the sticky mucus & cilia is a barrier of saline lubricant, preventing adhesion.

• Bronchioles and alveoli contain no mucus

Cilia move in waves to shunt mucus up and out of the trachea — mucociliary escalator.

• Once pharynx is reached, swallowed or coughed out

How its made?

Saline lubricant

NKCC transporter = 1 Na+, 1 K+, 2 Cl- ions moved

CFTR transporter = Moves Cl- ions into the lumen/cilia side

Na+ ions move across the cells to balance out Cl- ion movement

Now NaCl (salt) formed to make saline as water follows the movement of ions

Ppl with cystic fibrosis = no CFTR transporter, no Cl- ion movement, no saline produced

Atmospheric pressure

At sea level, 760 mmHg.

At HIGHER altitudes, atmospheric pressure DECREASES

Boyle’s law

p1v1 = p2v2

• Pressure is INVERSELY proportional to volume

volume up, pressure down

volume down, pressure up

Quiet breathing

Inspiration is an ACTIVE process - muscles are put into action

Expiration is a PASSIVE process - muscles relax

• Diaphragm

• External intercostals

• Elastic recoil from alveoli also play a part in increasing the pressure of lungs above atm pressure during exhalation

Quiet breathing: Pressure of pleural fluid, alvoli, and volume of air

Pleural fluid is subatmospheric - slightly below atmospheric pressure

During inspiration, pleural fluid decreases pressure even further as the ribs pull on the pleura which pulls on the lungs.

• But lungs have some resistance to being pulled and this decreases pleural pressure even further

Active expiration

During exercise, when we force more air out of our lungs each breath.

• Actively use inner intercostals and abdominal muscles

Physical factors effecting ventilation:

• Lung compliance

• Surface tension

• Pulmonary resistance

Physical ability for the lungs to stretch.

High compliance = High volume change for little pressure change = easier to inflate

Elastic recoil: Ability for lungs to resist being deformed/stretch.

• Elastic recoil = 1/compliance

  • High compliance = Low elastic recoil

  • e.g Alveoli have elastic, this helps for shape to recoil

    • If not present, easy to inflate (high compliance), but hard to deflate to original size (exhalation is hard = low elastic recoil)

High compliance = Low elastic recoil → EXHALE is HARD

Low compliance = High elastic recoil → INHALE is HARD

Physical factors effecting ventilation:

• Lung compliance

• Surface tension

• Pulmonary resistance

At any air-water interface the surface of the fluid is under tension due to the presence of hydrogen bonds.

Surfactants = Surface active agents = secreted by type 2 Alveolar cells

• Protein and phospholipid combo

• Disturbs surface tension of watery surface on alveoli

• Decreased surface tension = Easier to expand alveoli = increased compliance

Physical factors effecting ventilation:

• Lung compliance

• Surface tension

• Pulmonary resistance

Resistance of the respiratory system to air flow during inspiration and expiration.

From Poiseuille’s Law, only radius of airway can be changed.

From trachea → bronchi = Most resistance as little 90% of cross-sectional area

• However, cartilage rings keep airways open

From bronchioles → alveoli = Little resistance as HUGE cross-sectional area

Lung diseases:

• Restrictive lung disease – ventilation is restricted

• Obstructive lung disease – obstruction to ventilation

Due to decreased compliance of the lungs

• decreased ability to stretch, decreased ability to inhale

Causes:

• increased alveolar surface tension - decreased surfactant production

• Formation of inelastic tissue in the lung - Pulmonary fibrosis

  • Fibrous masses toughening up the lungs, likely due to occupational hazards like asbestos, coal mines, silica etc.

Lung diseases:

• Restrictive lung disease – ventilation is restricted

• Obstructive lung disease – obstruction to ventilation

Increased airway resistance. (i/e smaller airways)

• During exhalation, smaller airways can possibly collapse

• Decreased exhalation efficiency, decreased elastic recoil

  • CO2 remains trapped in lungs, poor O2 exchange

Asthma

Volume types in the lung

Tidal volume = Volume of air moved in and out for each quiet breath = 500 ml (REMEMBER)

Expiratory reserve volume (ERV) = Volume left remaining in lungs that can be exhaled after a quiet breath

Inspiratory reserve volume (IRV) = Extra volume that can be breathed into lungs after a quiet inhale

Residual volume = volume left after a full active exhale

Capacity types in the lung

• Sum of 2 or more volumes

Inspiratory capacity = TV + IRV = Total amount of air inhaled

Functional Residual capacity = ERV + RV = Amount of residual air in lungs after quiet exhale

Total lung capacity = TV + IRV + ERV + RV = Total max lung capacity

Vital capacity = TV + IRV + ERV = Total amount of exchangeable air in lungs

Forced vital capacity (FVC) and FEV1 = How much can you breath out FAST

• IF lower than normal indicative of asthma

Pulmonary ventilation/ minute ventilation

TOTAL volume of air moved into and out of the lungs each minute

• However, NOT all of this air is going to commit gas exchange, as not all reaches alveoli

Air in conducting zone = anatomical dead space = 150 ml (REMEMBER)

REMEMBER FORMULA

Alveolar ventilation

Volume of air that reaches the alveoli in 1 minute and undergoes gas exchange.

REMEMBER THE FORMULA

Dalton’s Law

Total pressure of a gas mixture is the sum of the partial pressure of the gases that the mixture

• Each gas in a mixture exerts its own pressure called its partial pressure (Pgas)

DALTON’s LAW DOES NOT ACCOUNT FOR WATER VAPOUR

Partial pressure of O2 in dry air vs humid air

REMEMBER FORMULAS

Humid air present inside lungs

Partial pressures of O2 & CO2 in blood

High CO2, low pH (acidic)

vice versa

Factors effecting alveolar ventilation

1. Enough O2 reaching alveoli

2. Enough gas exchange of CO2 & O2

3. Enough bloodflow to alveoli - “perfusion” of alveoli

Perfusion of lungs and alveoli

Usually 0.5L of blood in lungs at anytime.

BUT flow rate is high

Pulmonary arterial pressure is 25/8 mmHg vs 120/80 mmHg in systemic arteries

• Capillaries in the lungs are collapsible

• Enables only sections of the lungs to be actively perfused and used at rest, prevents waste of energy

if pCO2 increase, bronchioles dilate (more CO2 exhaled)

if pCO2 decreases, bronchioles constrict (less CO2 exhaled)

Hypoxia – decreased O2 levels in the blood

Hypercapnia – increased CO2 in the blood

• Can happen NOT at the same time

Emphysema = COPD

O2 consumption:

• Mass Balance (any gain must be offset by equal loss)

• Mass flow (how much O2 is transported around the body in 1 minutes)

QO2 = Oxygen consumption

• O2 is poorly soluble in blood, much more soluble with haemoglobin

• Haemoglobin can help blood carry 200ml/L of oxygen (4x what we need at rest)

  • Reserves left for sharp spikes in oxygen demand

  • Total blood O2 = dissolved O2 + O2 bound to Hb

1 haemoglobin molecule carries 4 iron that binds to 4 O2 molecules

• Can be fully or partially saturated

Law of mass action

When a reaction is at equilibrium, the ratio of products to the substrates is always the same

• If the ratio is disturbed by either adding or removing one of the participants of the reaction, the equation with shift to restore the equilibrium

Haemoglobin to pO2 graph

Decreased pH, increased temperature or increased PCO2 shift the curve to the right

(decreased affinity for O2 - more O2 given to body tissues)

Mimics exercise conditions (more acidic, more temp, more CO2)

CO2 transport

1. 7% dissolves in plasma

2. 93% diffuses into red blood cells (23% bind to haemoglobin — diff site from O2, 70% become HCO3- ions (acid))

HCO3- ions diffuse out of red blood cells in exchange for Cl- ions entering RBCs (chloride shift)

Neural control of breathing

Phrenic nerve involved somehow??

Motor neurons are ALWAYS firing — even when exhaling/relaxing in quiet breathing

Pre-Botzinger complex — pacemaker neurons that maintain quiet breathing pace

Ventilation rhythm — what keeps it in check?

• Peripheral chemoreceptors

• Central chemoreceptors

Mainly CO2 surprisingly, not O2 or pH

O2 still plays a part, but not as important.

Where? on Carotid arteries

Can INCREASE ventilation

Detect a decrease in PO2 or pH (more H+) or an increase in PCO2

• Send info to DRG

• Does not play a major role in maintaining ventialtion, major changes have to occur for anything notable

• Glomus cells trigger Ca2+ release after stimuli by Peripheral chemoreceptors, sends stimuli to DRG

Ventilation rhythm — what keeps it in check?

• Peripheral chemoreceptors

• Central chemoreceptors

Mainly CO2 surprisingly, not O2 or pH

O2 still plays a part, but not as important.

Where? on medulla

Can INCREASE or DECREASE ventilation

Detect ONLY changes in pCO2

• Senses pH changes in cerebrospinal fluid

If changes to pH are not rectified, Central chemoreceptors can become used to the pH change

• In chronic conditions (like COPD), oxygen becomes the main regulator of ventilation

Voluntary control via the limbic system cannot override involuntary chemoreceptor control of ventilation

Regulating pH

1. Chemical buffers - weak acids/bases (think carbonic acid HCO3-)

2. Respiratory responce - Peripheral & central chemoreceptors

3. Renal response -

   1. Proximal tubule: Overall↑HCO3 reabsorbed & ↓H+ secreted

   2. Distal tubule: I-cells 2 types

      1. Type A I-cells: ↑HCO3 reabsorbed & ↓H+ secreted — acidosis

      2. Type B I-cells: ↓HCO3 secreted & ↑H+ reabsorbed — alkalosis

Respiratory acidosis:

Hypoventilation

Hypoventilation → CO2 buildup → acidosis → causes like COPD (emphysema), bronchitis, improper muscle movement

How to fix? Renal Type A I-cells: ↑HCO3 reabsorbed & ↓H+ secreted — acidosis

Respiratory alkalosis:

Hyperventilation

Hyperventilation → Little CO2 → alkalosis → causes like panic attack, asthma, hypoxia from high altitude

How to fix? Renal Type B I-cells: ↓HCO3 secreted & ↑H+ reabsorbed — alkalosis

Metabilic acidosis

Think too much exercise, renal dysfunction (H+ improperly filtered out, buildup in body)

Compensated by respiratory or kidneys

Metabilic alkalosis

Causes like excessive vomiting (stomach acid lost too much), too much alkaline drugs

Compensated by respiratory or kidneys