scit 1408 applied human anatomy and physiology ii - respiratory system chapter 22 b
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SCIT 1408 Applied Human Anatomy and Physiology II - Respiratory System Chapter 22 BTRANSCRIPT
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Respiratory VolumesTV tidal vol
IRV Inspiratory
reserve volume
ERV Expiratory reserve volume
RV Residual volume
Amt air in or out @ rest; 500 ml
Amt air forcibly inhaled after TV; 2100-3200 ml
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
Max amt that can be expired after max. inspiration; total exchangeable air; TV+IRV+ERV; 4800 mls in young males
Amt air remaining in lungs after TV expiration; RV + ERV
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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: TLC FRC RV
Decreases: FEV
Restrictive disease Decreases:
VC TLC FRC RV
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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
Slow, deep breathing increases AVR and rapid, shallow breathing decreases AVR
AVR = frequency X (TV – dead space)
(ml/min) (breaths/min) (ml/breath)
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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: Dalton’s 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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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
Basic Properties of Gases: Henry’s Law
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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 (PO2) of venous blood
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
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 22.17
External resp:
O2 in/CO2 out
Air: alveoli: blood
O2 out/CO2 in
Tissues: blood
Oxygen/carbon dioxide exchanges follow gas partial pressure gradients
These gradients refer to plasma gas content, not gases bound to Hgb
Internal resp:O2 out/CO2 inTissues: blood
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Oxygenation of Blood
Figure 22.18
Rapid oxygenation of blood in pulmonary capillaries- 0.25 sec
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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
Figure 22.19
Reduced alveolar ventilation;excessive perfusion
Reduced alveolar ventilation;reduced perfusion
Pulmonary arteriolesserving these alveoliconstrict
Enhanced alveolar ventilation;inadequate perfusion
Enhanced alveolar ventilation;enhanced perfusion
Pulmonary arteriolesserving these alveolidilate
PO2
PCO2
in alveoli
PO2
PCO2
in alveoli
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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
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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 3–17
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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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Each Hb molecule binds 4 oxygen atoms Oxyhemoglobin (HbO2) Hemoglobin that has released oxygen is called
reduced or deoxyhemoglobin (HHb)
Oxygen Transport: Role of Hemoglobin
HHb + O2
Lungs
Tissues
HbO2 + H+
Fast & reversible rxn
Oxygen unloading Oxygen loading
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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
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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
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Only 20–25% 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
Hemoglobin Saturation Curve
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Hemoglobin Saturation Curve
Figure 22.20
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Other Factors Influencing Hb Saturation
Temperature, H+, PCO2, and BPG Modify the structure of hemoglobin and alter its
affinity for oxygen > in above:
< hb’s affinity for oxygen > oxygen unloading
< act in the opposite manner These parameters are all high in systemic
capillaries where oxygen unloading is the goal
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Other Factors Influencing Hemoglobin Saturation
Figure 22.21
In tissues, exercise > temp > unloading
In tissues, > C02, > unloading
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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
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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
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CO2 + H2O H2CO3 H+ + HCO3–
Carbon dioxide Water Carbonic
acidHydrogen
ionBicarbonate
ion
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
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
Figure 22.22a
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Transport and Exchange of Carbon Dioxide
Figure 22.22b
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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
Figure 22.23
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Influence of Carbon Dioxide on Blood pH The carbonic acid–bicarbonate 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+
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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 11–15
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Respiratory Control Centers
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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
Figure 22.25
1.
2.
3.5.
4.
6.
7.
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Depth and Rate of Breathing: PCO2
> levels detected by chemoreceptors in medulla > blood CO2 diffuses into cerebrospinal fluid
CSF cannot buffer the H+ & < pH; brain protection needed
PCO2 levels rise (hypercapnia):
increased depth and rate of breathing; return to homeostasis
CO2 + H2O H2CO3 H+ + HCO3–
Carbon dioxide Water Carbonic
acidHydrogen
ionBicarbonate
ion
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Depth and Rate of Breathing: PCO2
hyperventilation
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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
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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)
Depth and Rate of Breathing: PO2
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Peripheral Chemoreceptors
Figure 22.27
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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
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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
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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
Figure 22.28
genetic
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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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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
Lung Cancer
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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
Developmental Aspects
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Respiratory System Development
Figure 22.29
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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
Developmental Aspects