Respiratory System

Chapter 22

Role of Respiratory System

• Supplies body w/ O2 and disposes of CO2

• Four part process– Pulmonary ventilation

• Moving air in and out of lungs

– External respiration• Exchange of gases between lungs and blood

– Transport of respiratory gases• Moving air to and from tissues via blood

– Internal respiration• Exchange of gases between blood and tissues

Functional Respiratory System

• Conducting zone: carries air– Cleanses, humidifies, and warms air– Nose terminal bronchioles

• Respiratory zone: site of gas exchange– Respiratory bronchioles– Alveolar ducts– Alveoli

Nose and Nasal Cavity • Normal air entry, why not mouth?• Moistens, warms, and filters air– Superficial capillary beds– Vibrissae filter particulates– Respiratory epithelium (what is that?)

• Mucus traps debris and moves posterior to pharynx• Defensins and lysozymes

– Turbinate bones and meatuses enhance• Olfaction– Olfactory epithelia through cribriform plates– Nerve endings irritated = sneezing

• Resonation for speech

Pharynx

http://medical-dictionary.thefreedictionary.com/pharynx

• Nasopharynx– Air mov’t only

• Closed off by uvula w/ swallowing • Giggling prevents = nose expulsion

– Respiratory epithelium (why?)– Pharyngeal tonsil (adenoids)

• Oropharynx– Food and air mov’t– Stratified squamous (why?)– Palatine and lingual tonsils

• Laryngopharnx– Food and air mov’t– Stratified squamous – Branches to esophagus and larynx

Larynx

• Keep food and fluid out of lungs– Epiglottis (elastic) covers glottis

• Coughing/choking when fails

– False vocal cords• Transport air to lungs

– Supported by 8 hyaline cartilages• Voice production

– True vocal cords (elastic) vibrate as air passes• Pitch from vibration rate (more tension = faster = higher)• Loudness from force of expelled air (whisper = little/no vibration)

– Additional structures amplifies, enhances, and resonates– Pseudostratified ciliated columnar again (why?)

• Mucus up to pharynx

Trachea

• Transports air to lungs• Mucosal layer– Respiratory epithelium– Mucus trapped debris to pharynx

• Submucosal layer– Mucus glands

• Adventita– Connective tissue supported by C-rings of hyaline

cartilage

Bronchial Tree

Table 2: Divisions of the Bronchial Tree. Taken from Ross et al., Histology, a text and atlas, 10th edition, p. 589, Table 18.1.

The Respiratory Membrane

• Walls of the alveoli where actual exchange occurs– Simple squamous cells (type I cells)

surrounded by capillaries• Surface tension resists inflation– Cuboidal epithelia (type II cells) produce

surfactant to counter• Macrophages patrol – Dead/damage swept to pharynx

Lung Anatomy

• Paired air exchange organs– Right lung

• Superior, middle, and inferior lobes• Oblique and horizontal fissures

– Left lung• Superior and inferior lobes • Oblique fissure• Cardiac notch contributes to smaller size

• Costal, diaphragmatic, and mediastinal surfaces• Hilum where 1° bronchi and blood vessels enter

Pleura

• Serous membrane covering– Parietal pleura– Visceral pleura– Pleural fluid in cavity

• Reduces friction w/ breathing– Surface tension binds tightly– Expansion/recoil with thoracic cavity

• Creates 3 chambers to limit organ interferences

Pressure Relationships

• Relative to atmospheric pressure (Patm)– Sea level = 760 mmHg

• Intrapulmonary pressure (Ppul): pressure in alveoli

• Intrapleural pressure (Pip): pressure in pleural cavity– Always negative to Ppul

– Surface tension b/w pleura Lung wall

AtmospherePatm

Intrapleural fluid

Chest wall

Ppul Pip

(Ppul – Pip)

(Pat

m –

Ppu

l)

Transpulmonary Pressure (Ptp)

• Difference b/w intrapulmonary and intrapleural pressure (Ppul – Pip)– Influences lung size (Greater diff. = larger lungs)– Equalization causes collapse

• Keeps lungs from collapsing (parietal and visceral separation)– Alveolar surface tension and recoil favor aveoli

collapse– Recoil of chest wall pulls thorax out

Pulmonary Ventilation

• Inspiration and expiration change lung volume– Volume changes cause pressure

changes– Gases move to equalize

• Boyle’s Law– P1V1 = P2V2

• Increase volume = decrease pressure• Decrease volume = increase pressure

Patm – Ppul

RF =

Ppul < Patm

inspiration

Ppul > Patm

expiration

Breathing CycleInspiration Expiration• Thoracic cavity increases

– Pip decrease Ptp increase

• Lung volume increases– Ppul < Patm

• Air flows in till Ppul = Patm

• Inspiratory muscles relax• Thoracic cavity decreases

– Pip increase Ptp decrease

• Lung volume decreases– Ppul > Patm

• Air flows out till Ppul = Patm

Influencing Pulmonary Ventilation

• Airway resistance – Flow = pressure gradient/ resistance (F = P/R)– Diameter influences, but insignificantly

• Mid-sized bronchioles highest (larger = bigger, smaller = more)• Diffusion moves in terminal bronchioles (removes factor)

• Alveolar surface tension– Increase H20 cohesion and resists SA increase– Surfactants in alveoli disrupt = less E to oppose

• Lung compliance– ‘Stretchiness’ of the lungs– Stretchier lungs = easier to expand

• Tidal volume (TV): air moved in or out w/ one breath• Inspiratory reserve volume (IRV): forcible inhalation over TV• Expiratory reserve volume (ERV):forcible exhalation over TV• Residual volume: air left in lungs after forced exhalation

Pulmonary Volumes

Respiratory Capacities

• Inspiratory capacity (IC)– Inspired air after tidal expiration– TV + IRV

• Functional residual capacity (FRC)– Air left after tidal expiration– RV + ERV

• Vital capacity (VC)– Total exchangeable air– TV + IRV + ERV

• Total lung capacity (TLC)– All lung volumes– TV + IRV + ERV + RV

Non-Respiratory Air

• Dead space– Anatomical: volume of respiratory conducting passages– Alveolar: alveoli not acting in gas exchange– Total: sum of alveolar and anatomical

• Reflex movements– Cough: forcible exhalation through mouth– Sneeze: forcible exhalation through nose and mouth– Crying: inspiration and short expirations– Laughing: similar to crying– Hiccups: sudden inspiration from diaphragm spasms– Yawn: deep inspiration into all alveoli

Properties of Gases

• Dalton’s Law – Pressure exerted by each gas in a mix is independent of others

• PN2 ~ 78%, PO2 ~ 21% , PCO2 ~ .04

– Partial pressure (P) for each gas is directly proportional to its concentration• O2 at sea level 760mmHg x .21 = 160mmHg • 10,000 ft above 523mmHg x 0.21 = 110mmHg

• Henry’s Law– In contact w/ liquid, gas dissolves proportionately to partial

pressure• Higher partial pressure = faster diffusion• Equilibrium once partial pressure is equal

– Solubility and temperature can influence too (concentration)

External Respiration

• Gas exchange– Partial pressure gradients drive

• Alveoli w/ higher PO2 and tissues w/ PCO2

– PO2 gradients always steeper that PCO2

– PCO2 more soluble in plasma and alveolar fluid than PO2

– Equal amounts exchanged

• Respiratory membrane– Thin to allow mov’t– Moist to prevent desiccation– Large SA for diffusion amounts

External Respiration (cont.)

• Ventilation and perfusion synchronize to regulate gas exchange– PO2 changes arteriole diameter

• Low vasoconstriction redirect blood to higher PO2 alveoli

– PCO2 changes bronchiole diameter• High bronchiole dilation quicker removal of CO2

Oxygen Transport• 98% bound to hemoglobin as oxyhemoglobin (HbO2)

– Review structure– Deoxyhemoglobin (HHb) once O2 unloaded– Rest dissolved in plasma

• Affinity influenced by O2 saturation– 1st and 4th binding enhances– Previous unloading enhances

• Hemoglobin reversibly binds O2

– Influenced by PO2, temp., blood pH, PCO2, and [BPG]

HHb + O2

Lungs

TissuesHbO2 + H+

PO2 Influences on Hemoglobin

• Hb near saturation at lungs (PO2 ~ 100mmHg) and drops ~ 25% at tissues (PO2 ~ 40mmHg)– Hb unloads more O2 at lower

PO2

– Beneficial at high altitudes

• In lungs, O2 diffuses, Hb picks up = more diffusion– Hb bound O2 doesn’t

contribute to PO2

• Increase in [H+], PCO2, and temp

– Decrease Hb affinity for O2

• Enhance O2 unloading from the blood

– Areas where O2 unloading needed• Cellular respiration• Bohr effect from low pH and

increased PCO2

• Decreases have reverse effects

Controlling O2 Saturation

Carbon Dioxide Transport

• Small amounts (7 – 10%) dissolved in plasma• As carbaminohemoglobin (~20%)– No competition with O2 b/c of binding location

– HHb binds CO2 and buffers H+ better than HbO2, called the Haldane effect• Systemically, CO2 stimulates Bohr effect to facilitate

• In the lungs, O2 binds Hb releasing H+ to bind HCO3-

Carbon Dioxide Transport (cont.)

• Primarily (70%) as bicarbonate ions (HCO3-)

CO2 + H2O H2CO3 H+ + HCO3-

– Hb binds H+ = Bohr effect and little pH change– HCO3

- stored as a buffer against pH shifts in blood• Bind or release H+ depending on [H+]• CO2 build up (slow breathing) = H2CO3 up (acidity)

• Faster in RBC’s b/c carbonic anhydrase• Fig 22.22

Neural Control of Respiration

• Medullary respiratory centers– Dorsal respiratory group (DRG)

• Integrates peripheral signals• Signals VRG

– Ventral respiratory group (VRG)• Rhythm-generating and forced inspiration/expiration• Excites inspiratory muscle to contract

• Pontine center– Signals VRG– ‘Fine tunes’ breathing rhythm in sleep, speech, &

exercise

Regulating Respiration

• Chemical factors– Increase in PCO2 increases depth and rate

• Detected by central chemoreceptors (brainstem)• CO2 diffuses into CSF to release H+ (no buffering)

• Greater when PO2 and pH are lower

– Initial decrease in PO2 enhances PCO2 monitoring• Peripheral chemoreceptors in carotid and aortic bodies• Substantial drop to increase rate b/c Hb carrying capacity

– Declining arterial pH increases depth and rate • Peripheral chemoreceptors increase CO2 elimination

Regulating Respiration (cont.)

• Higher brain center influence– Hypothalamic controls

• Pain and strong emotion influence rate and depth• Increased temps. increases rate

– Cortical controls• Cerebral motor cortex bypasses medulla• Signals voluntary control (overridden by brainstem monitoring)

• Pulmonary irritant reflexes– Reflexive constriction of bronchioles– Sneeze or cough in nasal cavity or trachea/bronchi

• Inflation reflex– Stretch receptors activated w/inhalation– Inhibits inspiration to allow expiration

Homeostatic Imbalances• Sinusitis: inflamed sinuses from nasal cavity infection• Laryngitis: inflammation of vocal cords• Pleurisy: inflammation of pleural membranes, commonly from pneumonia• Atelectasis: lung collapse from clogged bronchioles• Pneumothorax: air in the intrapleural spaces• Dyspnea: difficult or labored breathing• Pneumonia: infectious inflammation of the lungs (viral or bacterial)• Emphysema: permanent enlargement of the alveoli due to destruction• Chronic bronchitis: inhaled irritants causing excessive mucus production• Asthma: bronchoconstriction prevents airflow into alveoli• Tuberculosis: an infectious disease (Mycobacterium tuberculosis) causing fibrous

masses in the lungs• Cystic fibrosis: increased mucus production which clogs respiratory passages• Hypoxia: inadequate O2 delivery

– Anemic (low RBC’s), ishemic (impaired blood flow), histotoxic (cells can’t use O2), hypoxemic (reduced arterial PO2

)