1. The Respiratory System
Chapter 22
G.R. Pitts, , Ph.D., J.R. Schiller, , Ph.D., and James F. Thompson, Ph.D.
Use the video clips: CH 22 – Upper Respiratory Anatomy and CH 22 – Lower Respiratory Anatomy for a review of respiratory system structure

2. Respiration Pulmonary ventilation External (pulmonary) respiration
Breathing - inspiration & expiration
External (pulmonary) respiration
Gas exchange between lung (alveoli) & blood
Transport of respiratory gases
Oxygen and carbon dioxide (CO2) must be transported between the tissues and the lungs
Internal (tissue) respiration
Gas exchange between blood and tissue cells
RBCs deliver O2 and pick up CO2 in the capillary beds
cells use O2 and produce CO2 (cellular respiration)

3. The Respiratory Tree
upper respiratory tract for ventilation (conduction of air)
lower respiratory tract for respiration (gas exchange by diffusion)

4. The Larynx Voice Production Vestibular folds (false vocal cords)
Vocal folds (true vocal cords)
during exhalation laryngeal muscles pull the folds across the opening and tense the folds
exhaled air induces vibrations which create sound waves
volume
pitch

5. Tracheotomy

6. Regulation of the Airway
Smooth muscle
Parasympathetic (ANS), allergic response - bronchoconstriction
Sympathetic (ANS) response - bronchodilation
histamine release
allergy/asthma

7. The Alveolar Space Alveolar fluid
Surface tension
Attraction of water to other water molecules
Surfactant: phospholipids decrease surface tension
Respiratory distress syndrome

8. The Pleural Cavities Lungs – housed in the bony thorax
Pleural problems
pneumothorax
hemothorax
pleurisy: inflammation
collapsed lung: atelectasis

9. Muscles For Ventilation
Muscles for inspiration
diaphragm
dome-shaped muscle forms inferior wall of thoracic cavity
muscle flattens when contracted, expanding thoracic cavity
minimal involvement in normal resting breathing
important for physical exertion and speech/singing
can be limited by tight clothing, pregnancy, obesity, edema
external intercostals
pull ribs upward, push sternum forward, expand thoracic cavity

10. Muscles For Ventilation
Muscles for expiration
internal intercostals
pull ribs downward, pull sternum inward, compress thoracic cavity
abdominals
compress abdominal and thoracic cavities

11. Pulmonary Ventilation
Exchange of gases between the atmosphere and the alveoli of the lung
Bulk flow of gases due to pressure differences
Lung air pressure is atmospheric (760 mm Hg at sea level)
need to create a pressure gradient for air flow into the lungs (Q=ΔP/R)
two mechanisms
increase atmospheric pressure (positive ventilation)
decrease lung air pressure (negative ventilation)
Structure & Function of thoracic cavity helps

12. Physics of Ventilation
Boyle’s law - pressure in a closed container is inversely proportional to the volume of container
Diaphragm, pleura and thoracic wall
At rest, volume decreased
During inspiration, volume increased

13. Ventilation Pressure Relationships
Intrapulmonary pressure (Ppul)
In alveoli
Variable, but equilibrates with atmospheric (760 mm Hg at sea level)
Intrapleural pressure (Pip)
Pleural cavity
Usually 4 mm Hg less that Ppul
Lungs have elastic recoil
Pleural fluid surface tension
Elasticity of chest wall
Transpulmonary pressure = (Ppul - Pip)

14. Pul. Ventilation - Inspiration
Pressure changes
With expansion of the rib cage and depression of the diaphragm, intrapulmonary pressure falls 1-2 mm Hg
Establishes a small negative pressure gradient permitting air flow into lungs

15. Pulmonary Ventilation - Expiration
Breathing out (expiration) also due to a pressure gradient
3 important factors:
relaxation of diaphragm (rises)
elastic recoil of chest wall and the lungs
surface tension the pleural and alveolar fluids of the lungs
Forced muscular expiration – oblique and transverse abdominals indirectly “compress" the lungs

16. Pulmonary Ventilation - Summary

17. Pulmonary Ventilation - Summary

18. Pulmonary Ventilation - Summary

19. Ventilation Assessment
Respiration (ventilation)
1 ventilatory cycle (1 inspiration and 1 expiration)
12 breaths/min (resting rate = RR)
minute ventilation - ~6 L/min
Pulmonary Volumes & Capacities
Spirometry: measures respiratory volumes on a spirogram (recording)
[Biopac exercises in lab]

20. Pulmonary Volumes (measured)
Tidal volume (TV)
350 mL reaches the alveoli
150 mL do not, this air is trapped in anatomical dead space
Inspiratory reserve volume (IRV)
Expiratory reserve volume (ERV)
Residual volume (RV) [~1 L]
FEV1 – forced expiratory volume in 1 second

21. Pulmonary Capacities (calculated)
Pulmonary capacities = sums of certain lung volumes
Inspiratory capacity (IC) = TV+IRV [~ 3600 mL]
Functional residual capacity (FRC) = ERV+RV
Vital capacity (VC) = IRV+TV+ERV [~4800 mL]
Total lung capacity (TLC) = sum of all volumes

22. Exchange of O2 & CO2 - Gas Laws
Dalton's law
Each gas in a mixture of gases exerts own pressure as if all other gases were not present
Atmospheric pressure = sum of all partial pressures (p) of atmospheric gases
atmospheric pressure at sea level mm Hg
N2 - 79% mm Hg
O2 - 21% mm Hg, 105 mm Hg in alveoli
CO % mm Hg
partial pressure difference with increasing altitude
10,000 ft mm Hg - pO2 110 mm Hg (67 mm Hg in alveoli)
20,000 ft mm Hg - pO2 = 73 mm Hg (40 mm Hg in alveoli)
50,000 ft - 87 mm Hg, pO2 = 18 mm Hg (2 mm Hg in alveoli)
partial pressure difference with diving depth under water
33 ft mm Hg - pO2 320 mm Hg (210 mm Hg in alveoli)
pressure increases 1 atmosphere for every 33 ft of increased depth

23. Exchange of O2 & CO2 - Gas Laws
Henry's law
Amount of a gas that dissolves in liquid is proportional to the partial pressure of gas and its solubility coefficient
Solubility coefficients for normal gases O2
0.024 ml O2 /mm Hg
2.5 ml O2 at atmospheric pressure
CO2
0.57 ml/mm Hg
high solubility, low % N2
0.012 ml/mm Hg
low solubility, high %
Nitrogen narcosis
Bends

24. Exchange of O2 and CO2
Gas exchange between alveoli & capillaries = external respiration
changing deoxygenated to oxygenated blood
rate of gas exchange is dependent on:
surface area for diffusion
diffusion distance
pressure gradient
breathing rate/depth

25. Exchange of O2 and CO2 (cont.)
Internal (tissue) respiration
O2 & CO2 exchange between capillaries and tissue cells
changing oxygenated to deoxygenated
Only 25% of the blood’s O2 enters the cells at rest
CO2 moves in the opposite direction
Diffusion is driven by pressure gradients (and concentration gradients)

26. O2 Transport In The Blood
O2 does not dissolve well in water
another mechanism is needed to carry O2
most O2 is carried bound to Hgb
20 ml O2/100 ml blood
0.3 ml dissolved
19.7 ml carried by Hgb

27. Oxygen-Hemoglobin Dissociation Curve
pO2 is the most important factor in O2/Hgb interaction
Cooperativity
p50 = 27 mm Hg
Terminology
partially saturated
fully saturated
percent saturation of hemoglobin
Affinity
O2 content
carrying capacity

28. O2 Transport (cont.)
Several other factors influence hemoglobin’s affinity for O2:
Acidity - Bohr effect
low/acid pH, lower affinity for O2
shifts the O2 affinity curve to the right
more PO2 for the same saturation
H+ binding changes Hgb’s structure, decreasing Hgb’s O2 affinity
pCO2
CO2 binds to Hgb
causes conformational changes in Hgb
CO2 binding to Hgb decreases the affinity of Hgb for O2
carbonic anhydrase & acidity

29. O2 Transport - Other Factors (cont.)
Temperature is inversely related to Hgb’s O2 affinity
Lower temperature encourages O2 uptake
higher temperature encourages O2 release
Increased BPG (RBC metabolic by-product) encourages O2 release
73%
50%

30. O2 Transport - Other Factors (cont.)
Fetal hemoglobin
increased affinity for O2 at all temperatures and pH levels compared to adult Hgb
allows fetus to obtain O2 from mother in conditions where adult Hgb would be releasing O2
Carbon monoxide (CO) poisoning
CO has 200 times greater affinity for Hgb than O2
blocks O2 transport - blocks Hgb’s ability to pick up or release O2

31. Hemoglobin-Nitric Oxide Partnership
Hemoglobin picks up oxygen and nitric oxide in the lungs
Oxygen dissociates from hemoglobin in the tissues
This causes nitric oxide release into the tissues
Nitric oxide is a vasodilator
Therefore, where O2 levels are low, hemoglobin releases O2 and a vasodilator which assists in O2 delivery
i.e., hemoglobin carries its own vasodilator

32. O2 Transport: Hypoxia (Low O2)
Hypoxic hypoxia
Low O2 due to low O2 in the lungs
Low O2 saturation
May be caused by low O2 in the atmosphere (altitude, smoke inhalation, etc.) or suffocation/strangulation
Anemic hypoxia
Low O2 due to low numbers of RBC's
Low O2 content
May be caused by any anemia, other hemolytic diseases, cancers and cancer treatments, malnutrition, etc.

33. O2 Transport: Hypoxia (Low O2)
Stagnant (ischemic) hypoxia
Low O2 due to reduced blood flow
Low O2 delivery
May be caused by heart failure, blood clot or other embolus
Histotoxic hypoxia
Tissues cannot use O2, usually due to the presence of a toxin or poison
May be caused by cyanide (cigarettes, chemicals), carbon monoxide (CO) (cigarettes, fires, automobile exhaust, etc.), botulinin toxin, etc.

34. CO2 transport 55 ml CO2 /100 ml blood Carried in 3 forms
Dissolved CO2 - 7% of total
Carbaminohemoglobin
23% of total
binds to the non-heme portion of Hemoglobin
Haldane Effect:
In the lungs, when O2 is available to bind to Hgb, Hgb has less affinity for binding CO2
This reverses in the tissue beds
Bicarbonate ions
70% of total
vital to survival
an important acid-base buffer

35. CO2 Transport (cont.)
The rate of bicarbonate formation is increased by the enzyme, carbonic anhydrase
CO2 +H20 ⇌ H2CO3- ⇌ HCO3- +H+
An equilibrium reaction
an excess of either one will shift the results in the other direction!
excess CO2 will result in increased H+ production and increased blood acidity
less CO2 will result in decreased H+ production and decreased blood acidity (or increased blood alkalinity)
Bicarbonate ion (HCO3-) is an important blood buffer

36. O2 and CO2 Transport - Summary
Gas exchange across the lung (external respiration)

37. O2 and CO2 Transport - Summary
Gas exchange in the tissues (internal respiration)

38. Nervous Control of Respiration
Neural control by medulla
2 regional centers exert homeostatic control
Medullary respiratory center
Determines basal respiratory rhythm
Ventral respiratory group
rhythm generating & integrating center
exhibits autorhythmic activity
Inspiratory neurons fire for inspiration (2 sec)
Expiratory neurons then fire (3 sec)
Eupnea – normal (tidal) breathing rate
VRG may cause gasping during severe hypoxia
Dorsal respiratory group
integrates information from stretch proprioceptors & chemoreceptors
sends output to VRG to cause more forceful ventilations when needed by activities

39. Neuronal Control of Breathing
Inspiratory neurons in the medullary respiratory center exhibit a rhythmic firing pattern.
Those impulses are transmitted to the diaphragm via the phrenic nerve and the intercostal muscles via the intercostal nerves.

40. Control of Respiration
Pontine respiratory center
Modifies DRG and VRG activity
Smoothes transition between inhalation and exhalation
Brain damage in this area causes prolonged inspirations (apneustic breathing) seen in some coma patients
Pontine respiratory group (formerly, pneumotaxic and apneustic areas)
Fine tunes breathing rhythm during activity
Speaking
Sleep
Exercise
Receives input from higher brain centers and peripheral receptors

41. Control of Respiration: Pulmonary Stretch Receptors
Blue tracing: with pulmonary stretch receptor input
Red tracing: No pulmonary stretch receptor input
Stretch receptors in the lungs cut off the activity of the inspiratory neurons in the medullary respiratory center to prevent overinflation (negative feedback)
[The reflex decrease in inspiration due to pulmonary stretch receptor activity is called the Hering-Breuer reflex]

42. Physiological Control of Respiration
Regulation of respiratory center activity
O2 is overrated!
Mainly a CO2 driven system unless pO2 <50 mm Hg
CO2 +H20 ⇌ H2CO3- ⇌ HCO3- +H+
Small  pCO2 (>40 mm Hg)
known as hypercapnea
results in hyperventilation
lowers pCO2 (negative feedback)
Small  pCO2 (<40 mm Hg)
known as hypocapnia
results in hypoventilation
raises pCO2 (negative feedback)
Cortical influences - determine respiration pattern
Voluntary control often works preventatively
Voluntary control has limits; it can be overridden by sensory inputs

43. Neuronal Control of Breathing
The medullary respiratory center increases activity in response to a rise in PaCO2 (alveolar CO2)

44. Regulating Resp. Center Activity
Other influences:
Chemoreceptors
Limbic system - anticipation of activity or emotional anxiety
Temperature -  temp  RR
Pain - sudden severe pain inhibits breathing
Irritation of air passages
mechanical/chemical irritation
cessation followed by coughing
Diving reflex with cold water on face  apnea
Stretching anal sphincter -  RR

45. Aging and the Respiratory System
Loss of elasticity of lung tissue
Decreased airway and alveolar elasticity decreases ventilation capacities
A 35% decrease in ventilation capacity can be expected by age 70

46. Chronic Obstructive Pulmonary Disease
Irreversible decrease in ventilation ability, esp. to exhale
Dyspnea - difficult and labored breathing
Coughing & frequent pulmonary infections
Respiratory failure – hypoventilation
Emphysema – permanent enlargement of alveoli and destruction of alveolar walls
Chronic bronchitis – inhaled irritants cause mucus production leading to inflammation and fibrosis of lower passageways
Asthma – usually of allergic origin

47. The Joys of Smoking!
Nicotine constricts terminal bronchioles decreasing air delivery to alveoli
Carbon monoxide binds to Hgb preventing O2 binding
Irritants in smoke increase mucous secretion and cause swelling in the bronchial tree
Irritants inhibit mucociliary elevator in the respiratory tree
Compounds in tobacco suppress the immune system (cyanide and others)
Eventually, smoking leads to alveolar destruction and emphysema or other chronic pulmonary obstructive dieseases (COPDs)
Tobacco tar contains potential carcinogens which may induce cancers

48. End Chapter 22