Transcript Chapter 22

Chapter 22
The Respiratory
System
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
Respiration
• Pulmonary ventilation
– 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)
The Respiratory Tree
• upper respiratory
tract for ventilation
(conduction of air)
• lower respiratory
tract for respiration
(gas exchange by
diffusion)
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
Tracheotomy
Regulation of the Airway
• Smooth muscle
– Parasympathetic
(ANS), allergic
response bronchoconstriction
– Sympathetic (ANS)
response bronchodilation
• histamine release
• allergy/asthma
The Alveolar Space
• Alveolar fluid
– Surface tension
– Attraction of
water to other
water molecules
• Surfactant:
phospholipids
decrease surface
tension
• Respiratory
distress
syndrome
The Pleural Cavities
• Lungs – housed in the
bony thorax
• Pleural problems
–
–
–
–
pneumothorax
hemothorax
pleurisy: inflammation
collapsed lung: atelectasis
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
Muscles For Ventilation
•Muscles for
expiration
internal
intercostals
• pull ribs downward,
pull sternum inward,
compress thoracic
cavity
abdominals
• compress abdominal
and thoracic cavities
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
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
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)
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
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
Pulmonary Ventilation - Summary
Pulmonary Ventilation - Summary
Pulmonary Ventilation - Summary
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]
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
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
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 - 760 mm Hg
– N2 - 79% - 600 mm Hg
– O2 - 21% - 160 mm Hg, 105 mm Hg in alveoli
– CO2 - 0.04% - 0.30 mm Hg
• partial pressure difference with increasing altitude
– 10,000 ft - 523 mm Hg - pO2 110 mm Hg (67 mm Hg in alveoli)
– 20,000 ft - 349 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 - 1520 mm Hg - pO2 320 mm Hg (210 mm Hg in alveoli)
– pressure increases 1 atmosphere for every 33 ft of increased depth
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
Exchange of O2 and CO2
•
Gas exchange
between alveoli &
capillaries = external
respiration
– changing
deoxygenated to
oxygenated blood
– rate of gas exchange
is dependent on:
1) surface area for
diffusion
2) diffusion distance
3) pressure gradient
4) breathing rate/depth
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)
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
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
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
O2 Transport - Other Factors (cont.)
• Temperature is
inversely related to
Hgb’s O2 affinity
• Lower temperature
encourages O2
uptake
73%
• higher temperature
encourages O2
50%
release
• Increased BPG
(RBC metabolic byproduct) encourages
O2 release
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
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
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.
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.
CO2 transport
• 55 ml CO2 /100 ml blood
• Carried in 3 forms
1. Dissolved CO2 - 7% of total
2. 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
3. Bicarbonate ions
• 70% of total
• vital to survival
• an important acid-base buffer
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
O2 and CO2 Transport - Summary
• Gas exchange across the lung (external respiration)
O2 and CO2 Transport - Summary
• Gas exchange in the tissues (internal respiration)
Nervous Control of Respiration
• Neural control by medulla
– 2 regional centers exert homeostatic control
1. 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
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.
Control of Respiration
2. 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
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]
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
Neuronal Control of Breathing
The medullary respiratory center
increases activity in response to a
rise in PaCO2 (alveolar CO2)
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
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
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
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
End Chapter 22