Transcript Respiratory System

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
• 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
http://medical-dictionary.thefreedictionary.com/pharynx
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
– Sea level = 760 mmHg
• Intrapulmonary pressure
(Ppul): pressure in alveoli
• Intrapleural pressure (Pip):
pressure in pleural cavity
Atmosphere
Patm
(Patm – Ppul)
• Relative to atmospheric
pressure (Patm)
Chest wall
Pip
Ppul
(Ppul – Pip)
– Always negative to Ppul
– Surface tension b/w pleura
Intrapleural fluid
Lung wall
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
Ppul < Patm
inspiration
• Boyle’s Law
– P1V1 = P2V2
• Increase volume = decrease pressure
• Decrease volume = increase pressure
Ppul > Patm
expiration
F=
Patm – Ppul
R
Breathing Cycle
Inspiration
• Thoracic cavity increases
– Pip decrease  Ptp increase
• Lung volume increases
– Ppul < Patm
• Air flows in till Ppul = Patm
Expiration
• 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
Pulmonary Volumes
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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
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
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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
Lungs
HHb + O2
HbO2 + H+
Tissues
– Influenced by PO2, temp., blood pH, PCO2, and [BPG]
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
Controlling O2 Saturation
• 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
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
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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)