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Respiratory Volumes

TV tidal vol

Amt air in or out @ rest; 500 ml

IRV Inspiratory

Amt air forcibly inhaled after TV; 2100-3200 ml

reserve volume

ERV Expiratory
reserve volume

RV Residual
volume

Amt air forcibly exhaled after TV; 1000-1200 ml


Amt air still in lungs after forceful expiration;
1200 ml

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Respiratory Capacity
IC

Inspiratory
capacity

FRC

Functional
residual capacity

VC

Vital capacity

Max. amt that can be inspired after TV


expiration; TV + IRV
Amt air remaining in lungs after TV expiration;
RV + ERV

Max amt that can be expired after max.


inspiration; total exchangeable air;
TV+IRV+ERV; 4800 mls in young males

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Dead Space

Anatomical dead space volume of air in the


conducting respiratory passages (150 ml)

Alveolar dead space alveoli that cease to act in


gas exchange due to collapse or obstruction

Total dead space sum of alveolar and anatomical


dead spaces; not available for gas exchange

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Pulmonary Function Tests

Spirometry evaluates respiratory function; DX between


Obstructive & Restrictive Disease

Obstructive - increased airway resistance;

Example: Chronic bronchitis

> TLC, FRC, RV

Restrictive - reduction in total lung capacity;

Asbestosis, TB

< VC, TLC, FRC, RV

FVC amt air expelled after taking deep breath & forceful
exhalation; reduced FEV in obstructive diseases

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Pulmonary Function Tests

Obstructive disease

Increases:

Restrictive disease

Decreases:

TLC

VC

FRC

TLC

RV

FRC

Decreases:

RV

FEV

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Alveolar Ventilation

Alveolar ventilation rate (AVR) measures the


flow of fresh gases into and out of the alveoli
during a particular time
AVR
(ml/min)

frequency
(breaths/min)

(TV dead space)


(ml/breath)

Slow, deep breathing increases AVR and rapid,


shallow breathing decreases AVR

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Nonrespiratory Air Movements

Most result from reflex action

Examples include: coughing, sneezing, crying,


laughing, hiccupping, and yawning

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Basic Properties of Gases:


Daltons Law of Partial Pressures
Total pressure exerted by a mixture of gases is the
sum of the pressures exerted independently by
each gas in the mixture

The partial pressure of each gas is directly


proportional to its percentage in the mixture

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Basic Properties of Gases: Henrys Law

When a mixture of gases is in contact with a liquid,


each gas will dissolve in the liquid in proportion to
its partial pressure and its solubility

Carbon dioxide: > soluble

Oxygen: < (1/20th) soluble

Nitrogen is practically insoluble in plasma

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Composition of Alveolar Gas

The atmosphere = > oxygen & nitrogen

Alveoli = > carbon dioxide & water vapor

These differences from:

Gas exchanges in the lungs oxygen diffuses from


the alveoli and carbon dioxide diffuses into the
alveoli

Humidification of air by conducting passages

The mixing of alveolar gas that occurs with each


breath

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External Respiration: Pulmonary Gas


Exchange

Factors influencing the movement of oxygen and


carbon dioxide across the respiratory membrane
1. Partial pressure gradients and gas solubilities
2. Matching of alveolar ventilation and pulmonary
blood perfusion
3. Structural characteristics of the respiratory
membrane

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Partial Pressure Gradients and Gas


Solubilities
The partial pressure oxygen (PO ) of venous blood
2
is 40 mm Hg; the partial pressure in the alveoli is
104 mm Hg

This steep gradient allows oxygen partial pressures


to rapidly reach equilibrium (in 0.25 seconds), and
thus blood can move three times as quickly (0.75
seconds) through the pulmonary capillary and still
be adequately oxygenated

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Partial Pressure Gradients and Gas


Solubilities
Although carbon dioxide has a lower partial
pressure gradient:

It is 20 times more soluble in plasma than oxygen

It diffuses in equal amounts with oxygen

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External resp:
O2 in/CO2 out
Air: alveoli: blood

Oxygen/carbon
dioxide exchanges
follow gas partial
pressure gradients
These gradients
refer to plasma gas
content, not gases
bound to Hgb

O2 out/CO2 in
Tissues: blood
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Internal resp:
O2 out/CO2 in
Tissues: blood
Figure 22.17

Oxygenation of Blood
Rapid oxygenation of blood in pulmonary
capillaries- 0.25 sec

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Figure 22.18

Ventilation-Perfusion Coupling

Ventilation amt gas reaching alveoli

Perfusion blood flow to alveoli

Ventilation and perfusion must be tightly regulated


for efficient gas exchange

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Ventilation-Perfusion Coupling

Autoregulation in pulmonary arterioles: (opposite from all


other arterioles in the circulation)

If PO2 is low, arterioles constrict

If PO2 is high, arterioles dilate

PCO2 in alveoli cause changes in the diameters of the


bronchioles

In passageways where alveolar PCO2 is high, bronchioles


dilate
In passageways where alveolar PCO2 PCO2 is low,
bronchioles constrict

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Ventilation-Perfusion Coupling
PO2
PCO2
in alveoli
Reduced alveolar ventilation;
excessive perfusion

Pulmonary arterioles Reduced alveolar ventilation;


serving these alveoli reduced perfusion
constrict

PO2
PCO2
in alveoli

Enhanced alveolar ventilation;


inadequate perfusion

Pulmonary arterioles Enhanced alveolar ventilation;


serving these alveoli enhanced perfusion
dilate

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Figure 22.19

Surface Area and Thickness of the


Respiratory Membrane

Respiratory membranes

0.5 - 1 m thick; allows efficient gas exchange

>>> surface area

Wet lungs, edema = thickened membranes, < gas


exchange

Emphysema,walls of adjacent alveoli break


through, decrease surface area, < gas exchange

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Internal Respiration

The factors promoting gas exchange between


systemic capillaries and tissue cells are the same as
those acting in the lungs

The partial pressures and diffusion gradients are


reversed

PO2 in tissue is always lower than in systemic


arterial blood

PO2 of venous blood draining tissues is 40 mm Hg


and PCO2 is 45 mm Hg

PLAY

InterActive Physiology :
Respiratory System: Gas Exchange, page 317

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Oxygen Transport

Molecular oxygen is carried in the blood:

98.5 % Bound to hemoglobin (Hb) in RBCs

Rest is dissolved in plasma

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Oxygen Transport: Role of Hemoglobin

Each Hb molecule binds 4 oxygen atoms

Oxyhemoglobin (HbO2)

Hemoglobin that has released oxygen is called


reduced or deoxyhemoglobin (HHb)
Fast & reversible rxn
Oxygen unloading

Lungs

HHb + O2

Oxygen loading

HbO2 + H+
Tissues

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Hemoglobin (Hb)

Saturated hemoglobin four O2 bound (1 to each


heme)

Partially saturated hemoglobin 1, 2, or 3 O2 bound

After the first O2 binds or unbinds, others bind or


unbind more quickly; (affinity increases with
degree of saturation)

The rate that hemoglobin binds and releases oxygen


is regulated by:

PO2, temperature, blood pH, PCO2, and the


concentration of BPG (biphosphoglycerate)

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Influence of PO2 on Hemoglobin Saturation

Oxygen-hemoglobin dissociation curve =


Hemoglobin saturation plotted against PO2

98% saturated arterial blood contains 20 ml


oxygen per 100 ml blood (20 vol %)

As arterial blood flows through capillaries, 5 ml


oxygen are released

The saturation of hemoglobin in arterial blood


explains why breathing deeply increases the PO2
but has little effect on oxygen saturation in
hemoglobin

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Hemoglobin Saturation Curve

Hemoglobin is almost completely saturated at a PO2


of 70 mm Hg

Further increases in PO2 produce only small


increases in oxygen binding

Further, even when PO2 is below normal levels,


oxygen loading and delivery to tissues is ok &
unloading is stimulated by < PO2

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Hemoglobin Saturation Curve

Only 2025% of bound oxygen is unloaded during


one systemic circulation

If oxygen levels in tissues drop:

More oxygen dissociates from hemoglobin and is


used by cells

Respiratory rate or cardiac output need not increase

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Hemoglobin Saturation Curve

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Figure 22.20

Other Factors Influencing Hb Saturation

Temperature, H+, PCO2, and BPG

Modify the structure of hemoglobin and alter its


affinity for oxygen

> in above:

< hbs affinity for oxygen

> oxygen unloading

< act in the opposite manner

These parameters are all high in systemic


capillaries where oxygen unloading is the goal

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Other Factors Influencing Hemoglobin


Saturation

In tissues, exercise >


temp > unloading
In tissues, > C02, > unloading
Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Figure 22.21

Factors That Increase Release of Oxygen by


Hemoglobin
As cells metabolize glucose, carbon dioxide is
released into the blood causing:

Increases in PCO2 and H+ concentration in capillary


blood

Declining pH (acidosis), which weakens the


hemoglobin-oxygen bond (Bohr effect)

Metabolizing cells have heat as a byproduct and


the rise in temperature increases BPG synthesis

All these factors ensure oxygen unloading in the


vicinity of working tissue cells

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Carbon Dioxide Transport

Carbon dioxide: in blood in 3 forms

7-10% dissolved in plasma

20% bound to hemoglobin as carbaminohemoglobin

70% (HCO3) Bicarbonate ion in plasma

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Transport and Exchange of Carbon Dioxide

Carbon dioxide diffuses into RBCs and combines


with water to form carbonic acid (H2CO3), which
quickly dissociates into hydrogen ions and
bicarbonate ions
CO2
Carbon
dioxide

H2 O

Water

H2CO3
Carbonic
acid

H+
Hydrogen
ion

HCO3
Bicarbonate
ion

In RBCs, carbonic anhydrase reversibly catalyzes


the conversion of carbon dioxide and water to
carbonic acid

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Transport and Exchange of Carbon Dioxide

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Figure 22.22a

Transport and Exchange of Carbon Dioxide

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Figure 22.22b

Haldane Effect

< PO2, & < hb saturation = > CO2 can be carried in


the blood

In tissues, as > CO2 enters the blood:

> oxygen dissociates from hemoglobin (Bohr


effect)

> CO2 combines with hemoglobin, > HCO3

This situation is reversed in pulmonary circulation

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Haldane Effect

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Figure 22.23

Influence of Carbon Dioxide on Blood pH

The carbonic acidbicarbonate buffer system


resists blood pH changes

If hydrogen ion concentrations in blood begin to


rise, excess H+ is removed by combining with
HCO3

If hydrogen ion concentrations begin to drop,


carbonic acid dissociates, releasing H+

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Influence of Carbon Dioxide on Blood pH

Changes in respiratory rate can also:

Alter blood pH

Provide a fast-acting system to adjust pH when it is


disturbed by metabolic factors

PLAY

InterActive Physiology :
Gas Transport, pages 1115

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Respiratory Control Centers

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Figure 22.24

Depth and Rate of Breathing

Inspiratory depth- how much respiratory center


stimulates respiratory muscles

Rate of respiration- how long inspiratory center is


active

Respiratory centers in the pons and medulla are


sensitive to both excitatory and inhibitory stimuli

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Depth and Rate of Breathing- chemical regulation

Most important = arterial blood levels of:

CO2

O2

H+

Levels detected by:

Central chemoreceptors medulla

Peripheral chemoreceptors- aortic arch & carotids

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Neural & Chemical Influences on Brain Stem


Respiratory Centers
2.

1.

7.
4.

6.

5.

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3.

Figure 22.25

Depth and Rate of Breathing: PCO2

> levels detected by chemoreceptors in medulla

> blood CO2 diffuses into cerebrospinal fluid


CO2

Carbon
dioxide

H2 O
Water

H2CO3
Carbonic
acid

H+

Hydrogen
ion

HCO3
Bicarbonate
ion

CSF cannot buffer the H+ & < pH; brain protection needed

PCO2 levels rise (hypercapnia):

increased depth and rate of breathing;

return to homeostasis

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Depth and Rate of


Breathing: PCO2

hyperventilation

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Figure 22.26

Depth and Rate of Breathing: PCO2

Hypoventilation slow and shallow breathing due


to abnormally low PCO2 levels

Apnea (breathing cessation) may occur until PCO2


levels rise

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Depth and Rate of Breathing: PO2

Peripheral chemoreceptors monitor arterial O2

< PO2 (to 60 mm Hg) before O2 is stimulus for


increased ventilation

If CO2 not removed (emphysema, chronic


bronchitis), chemoreceptors adapt, become
unresponsive to < PCO2

Then, PO2 levels become the principal respiratory


stimulus (hypoxic drive)

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Peripheral Chemoreceptors

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Figure 22.27

Depth and Rate of Breathing: Arterial pH

< pH or Acidosis may reflect:

Carbon dioxide retention

Accumulation of lactic acid

Excess fatty acids in patients with diabetes mellitus

Respiratory system controls will attempt to raise


the pH by increasing respiratory rate and depth
even if O2 & CO2 levels are ok

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Respiratory Adjustments: Exercise


From intensity and duration of exercise

Vigorous exercise:

> Ventilation - 20 fold

Breathing- deeper and more vigorous

Respiratory rate may by unchanged

Above is called Hyperpnea

Exercise-enhanced breathing is not prompted by an


increase in PCO2 or a decrease in PO2 or pH

These levels remain surprisingly constant during


exercise

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Respiratory Adjustments: High Altitude

Move quickly above 8000 ft

acute mountain sickness headache, shortness of


breath, nausea, and dizziness

Acclimatization

Increased ventilation 2-3 L/min higher than at sea


level

Chemoreceptors become more responsive to PCO2

Substantial decline in PO2 stimulates peripheral


chemoreceptors

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Chronic Obstructive Pulmonary Disease


(COPD)
Chronic bronchitis and obstructive emphysema

Pts have a history of:

Smoking

Dyspnea, where labored breathing occurs and gets


progressively worse

Coughing, frequent pulmonary infections

Respiratory failure, hypoxemia, carbon dioxide


retention, and respiratory acidosis

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Pathogenesis of COPD
genetic

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Figure 22.28

Asthma

Characterized by dyspnea, wheezing, and chest


tightness

Active inflammation of the airways precedes


bronchospasms

Airway inflammation is an immune response


caused by release of IL-4 and IL-5, which
stimulate IgE and recruit inflammatory cells

Airways thickened with inflammatory exudates


magnify the effect of bronchospasms

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Tuberculosis

Infectious disease caused by the bacterium


Mycobacterium tuberculosis

Symptoms include fever, night sweats, weight loss,


a racking cough, and splitting headache

Treatment requires a 12-month course of


antibiotics

High in homeless population; low compliance


due to length of treatment

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Lung Cancer

Accounts for 1/3 of all cancer deaths in the U.S.

90% of all patients with lung cancer were smokers

The three most common types are:

Squamous cell carcinoma (20-40% of cases) arises


in bronchial epithelium

Adenocarcinoma (25-35% of cases) originates in


peripheral lung area

Small cell carcinoma (20-25% of cases) contains


lymphocyte-like cells that originate in the primary
bronchi and subsequently metastasize

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Developmental Aspects

Mucosae of the bronchi and lung alveoli are


present by the 8th week

By the 28th week, a baby born prematurely can


breathe on its own; < surfactant before this

During fetal life, the lungs are filled with fluid and
blood bypasses the lungs

Gas exchange takes place via the placenta

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Respiratory System Development

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Figure 22.29

Developmental Aspects

At birth, respiratory centers are activated, alveoli


inflate, and lungs begin to function

Respiratory rate is highest in newborns and


slows until adulthood

Lungs continue to mature and more alveoli are


formed until young adulthood; teen smoking leads
to < alveoli; irreversible deficit

Respiratory efficiency decreases in old age

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

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