Marieb EN. Human Anatomy and Physiology 6th ed. The Respiratory System. Pearson Inc.
Cummings: 2004
Presented by: Afadiyanti, A. UNDIP Slide PPT by: Austin, V. University of Kentucky
Respiratory System
Consists of the respiratory and conducting zones Respiratory zone
Site of gas exchange Consists of bronchioles, alveolar ducts, and alveoli
Respiratory System
Conducting zone
Provides rigid conduits for air to reach the sites of gas exchange
Includes all other respiratory structures (e.g., nose, nasal cavity, pharynx, trachea)
Respiratory muscles diaphragm and other muscles that promote ventilation
Respiratory System
Figure 22.1
Airway to Alveoli
Alveoli to Red Blood Cell
Major Functions of the Respiratory System
To supply the body with oxygen and dispose of carbon dioxide Respiration four distinct processes must happen
Pulmonary ventilation moving air into and out of the lungs
External respiration gas exchange between the lungs and the blood
Major Functions of the Respiratory System
Transport transport of oxygen and carbon dioxide between the lungs and tissues
Internal respiration gas exchange between systemic blood vessels and tissues
Breathing
Breathing, or pulmonary ventilation, consists of two phases
Inspiration air flows into the lungs
Expiration gases exit the lungs
Pressure Relationships in the Thoracic Cavity
Respiratory pressure is always described relative to atmospheric pressure Atmospheric pressure (Patm)
Pressure exerted by the air surrounding the body Negative respiratory pressure is less than Patm Positive respiratory pressure is greater than Patm
Pressure Relationships in the Thoracic Cavity
Intrapulmonary pressure (Ppul) pressure within the alveoli
Intrapleural pressure (Pip) pressure within the pleural cavity
Pressure Relationships
Intrapulmonary pressure and intrapleural pressure fluctuate with the phases of breathing
Intrapulmonary pressure always eventually equalizes itself with atmospheric pressure Intrapleural pressure is always less than intrapulmonary pressure and atmospheric pressure
Pressure Relationships
Two forces act to pull the lungs away from the thoracic wall, promoting lung collapse
Elasticity of lungs causes them to assume smallest possible size Surface tension of alveolar fluid draws alveoli to their smallest possible size
Opposing force elasticity of the chest wall pulls the thorax outward to enlarge the lungs
Pressure Relationships
Figure 22.12
Pressure changes
Lung Collapse
Caused by equalization of the intrapleural pressure with the intrapulmonary pressure
Transpulmonary pressure keeps the airways open
Transpulmonary pressure difference between the intrapulmonary and intrapleural pressures (Ppul Pip)
Pulmonary Ventilation
A mechanical process that depends on volume changes in the thoracic cavity
Volume changes lead to pressure changes, which lead to the flow of gases to equalize pressure
Diaphragm
Intercostals
Inspiration
The diaphragm and external intercostal muscles (inspiratory muscles) contract and the rib cage rises
The lungs are stretched and intrapulmonary volume increases Intrapulmonary pressure drops below atmospheric pressure (1 mm Hg) Air flows into the lungs, down its pressure gradient, until intrapleural pressure = atmospheric pressure
Inspiration
Figure 22.13.1
Expiration
Inspiratory muscles relax and the rib cage descends due to gravity
Thoracic cavity volume decreases
Elastic lungs recoil passively and intrapulmonary volume decreases Intrapulmonary pressure rises above atmospheric pressure (+1 mm Hg) Gases flow out of the lungs down the pressure gradient until intrapulmonary pressure is 0
Expiration
Figure 22.13.2
Airway Resistance
As airway resistance rises, breathing movements become more strenuous
Severely constricted or obstructed bronchioles:
Can prevent life-sustaining ventilation Can occur during acute asthma attacks which stops ventilation
Epinephrine release via the sympathetic nervous system dilates bronchioles and reduces air resistance
Alveolar Surface Tension
Surface tension the attraction of liquid molecules to one another at a liquid-gas interface The liquid coating the alveolar surface is always acting to reduce the alveoli to the smallest possible size Surfactant, a detergent-like complex, reduces surface tension and helps keep the alveoli from collapsing
FUNCTIONS OF SURFACTANT
Surface tension related: 1. Packaging and release of surfactant from type II cells 2. Delivery and spreading of phospholipid at air/water surface 3. Aggregation of phospholipid at air/water surface 4. Removal of sufactant by type II cells and M
Airway defense related: 1. Opsinization of bacteria 2. Chemotaxis of leukocytes 3. Stimulation of phagocytosis by macrophages 4. Stimulates production of proinflammatory cytokines
surfactant molecule
alveolar surface area
Expiration surface area surfactant concentration surface tension Inspiration surface area surfactant concentration surface tension
Lung Compliance
The ease with which lungs can be expanded
Specifically, the measure of the change in lung volume that occurs with a given change in transpulmonary pressure Determined by two main factors
Distensibility of the lung tissue and surrounding thoracic cage Surface tension of the alveoli
Factors That Diminish Lung Compliance
Scar tissue or fibrosis that reduces the natural resilience of the lungs
Blockage of the smaller respiratory passages with mucus or fluid
Reduced production of surfactant Decreased flexibility of the thoracic cage or its decreased ability to expand
Factors That Diminish Lung Compliance
Examples include:
Deformities of thorax Ossification of the costal cartilage Paralysis of intercostal muscles
Respiratory Membrane
This air-blood barrier is composed of:
Alveolar and capillary walls
Their fused basal laminas
Alveolar walls:
Are a single layer of type I epithelial cells Permit gas exchange by simple diffusion Secrete angiotensin converting enzyme (ACE)
Type II cells secrete surfactant
Respiratory Membrane
Figure 22.9b
Respiratory Membrane
Figure 22.9.c, d
Surface Area and Thickness of the Respiratory Membrane
Respiratory membranes:
Are only 0.5 to 1 m thick, allowing for efficient gas exchange Have a total surface area (in males) of about 60 m2 (40 times that of ones skin) Thicken if lungs become waterlogged and edematous, whereby gas exchange is inadequate and oxygen deprivation results Decrease in surface area with emphysema, when walls of adjacent alveoli break through
SPIROMETER
nose clip
water
LUNG VOLUMES
volume ml
6000
inspiratory reserve volume
inspiratory capacity
vital capacity
total lung capacity
2900 2400
tidal volume expiratory reserve volume residual volume functional residual capacity FRC
1200
time
lung volume
inspiration active
expiration passive
expiration active
inspiration passive
FRC - functional residual capacity
time
Respiratory Volumes
Tidal volume (TV) air that moves into and out of the lungs with each breath (approximately 500 ml) Inspiratory reserve volume (IRV) air that can be inspired forcibly beyond the tidal volume (2100 3200 ml) Expiratory reserve volume (ERV) air that can be evacuated from the lungs after a tidal expiration (10001200 ml) Residual volume (RV) air left in the lungs after strenuous expiration (1200 ml)
Respiratory Capacities
Inspiratory capacity (IC) total amount of air that can be inspired after a tidal expiration (IRV + TV)
Functional residual capacity (FRC) amount of air remaining in the lungs after a tidal expiration (RV + ERV) Vital capacity (VC) the total amount of exchangeable air (TV + IRV + ERV) Total lung capacity (TLC) sum of all lung volumes (approximately 6000 ml in males)
Dead Space
Anatomical dead space volume of 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
Pulmonary Function Tests
Spirometer an instrument consisting of a hollow bell inverted over water, used to evaluate respiratory function Spirometry can distinguish between:
Obstructive pulmonary disease increased airway resistance
Restrictive disorders reduction in total lung capacity from structural or functional lung changes
Pulmonary Function Tests
Total ventilation total amount of gas flow into or out of the respiratory tract in one minute Forced vital capacity (FVC) gas forcibly expelled after taking a deep breath Forced expiratory volume (FEV) the amount of gas expelled during specific time intervals of the FVC
Pulmonary Function Tests
Increases in TLC, FRC, and RV may occur as a result of obstructive disease
Reduction in VC, TLC, FRC, and RV result from restrictive disease
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) X (TV dead space) (ml/breath)
Slow, deep breathing increases AVR and rapid, shallow breathing decreases AVR
Nonrespiratory Air Movements
Most result from reflex action
Examples include: coughing, sneezing, crying, laughing, hiccupping, and yawning
Composition of Alveolar Gas
The atmosphere is mostly oxygen and nitrogen, while alveoli contain more carbon dioxide and water vapor
These differences result 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
External Respiration: Pulmonary Gas Exchange
Factors influencing the movement of oxygen and carbon dioxide across the respiratory membrane
Partial pressure gradients and gas solubilities Matching of alveolar ventilation and pulmonary blood perfusion
Structural characteristics of the respiratory membrane
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
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
Partial Pressure Gradients
Figure 22.17
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
Oxygen Transport
Molecular oxygen is carried in the blood:
Bound to hemoglobin (Hb) within red blood cells Dissolved in plasma
Oxygen Transport: Role of Hemoglobin
Each Hb molecule binds four oxygen atoms in a rapid and reversible process
The hemoglobin-oxygen combination is called oxyhemoglobin (HbO2)
Hemoglobin that has released oxygen is called reduced hemoglobin (HHb) Lungs HHb + O2 HbO2 + H+
Tissues
Hemoglobin (Hb)
Saturated hemoglobin when all four hemes of the molecule are bound to oxygen Partially saturated hemoglobin when one to three hemes are bound to oxygen The rate that hemoglobin binds and releases oxygen is regulated by:
PO2, temperature, blood pH, PCO2, and the concentration of BPG (an organic chemical)
These factors ensure adequate delivery of oxygen to tissue cells
Influence of PO2 on Hemoglobin Saturation
Hemoglobin saturation plotted against PO2 produces a oxygen-hemoglobin dissociation curve
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
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 Oxygen loading and delivery to tissue is adequate when PO2 is below normal levels
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
Hemoglobin Saturation Curve
Figure 22.20
Other Factors Influencing Hemoglobin Saturation
Temperature, H+, PCO2, and BPG
Modify the structure of hemoglobin and alter its affinity for oxygen Increases of these factors:
Decrease hemoglobins affinity for oxygen
Enhance oxygen unloading from the blood Decreases act in the opposite manner
These parameters are all high in systemic capillaries where oxygen unloading is the goal
Other Factors Influencing Hemoglobin Saturation
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
Hemoglobin-Nitric Oxide Partnership
Nitric oxide (NO) is a vasodilator that plays a role in blood pressure regulation
Hemoglobin is a vasoconstrictor and a nitric oxide scavenger (heme destroys NO) However, as oxygen binds to hemoglobin:
Nitric oxide binds to a cysteine amino acid on hemoglobin
Bound nitric oxide is protected from degradation by hemoglobins iron
Hemoglobin-Nitric Oxide Partnership
The hemoglobin is released as oxygen is unloaded, causing vasodilation As deoxygenated hemoglobin picks up carbon dioxide, it also binds nitric oxide and carries these gases to the lungs for unloading
Carbon Dioxide Transport
Carbon dioxide is transported in the blood in three forms
Dissolved in plasma 7 to 10% Chemically bound to hemoglobin 20% is carried in RBCs as carbaminohemoglobin
Bicarbonate ion in plasma 70% is transported as bicarbonate (HCO3)
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 + H2O 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
Transport and Exchange of Carbon Dioxide
Figure 22.22a
Transport and Exchange of Carbon Dioxide
At the tissues:
Bicarbonate quickly diffuses from RBCs into the plasma The chloride shift to counterbalance the outrush of negative bicarbonate ions from the RBCs, chloride ions (Cl) move from the plasma into the erythrocytes
Transport and Exchange of Carbon Dioxide
At the lungs, these processes are reversed
Bicarbonate ions move into the RBCs and bind with hydrogen ions to form carbonic acid Carbonic acid is then split by carbonic anhydrase to release carbon dioxide and water
Carbon dioxide then diffuses from the blood into the alveoli
Transport and Exchange of Carbon Dioxide
Figure 22.22b
Haldane Effect
The amount of carbon dioxide transported is markedly affected by the PO2 Haldane effect the lower the PO2 and hemoglobin saturation with oxygen, the more carbon dioxide can be carried in the blood
Haldane Effect
At the tissues, as more carbon dioxide enters the blood:
More oxygen dissociates from hemoglobin (Bohr effect) More carbon dioxide combines with hemoglobin, and more bicarbonate ions are formed
This situation is reversed in pulmonary circulation
Haldane Effect
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+
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
Summary of gas transport
Control of Respiration: Medullary Respiratory Centers
The dorsal respiratory group (DRG), or inspiratory center:
Is located near the root of nerve IX Appears to be the pacesetting respiratory center Excites the inspiratory muscles and sets eupnea (12-15 breaths/minute)
Becomes dormant during expiration
The ventral respiratory group (VRG) is involved in forced inspiration and expiration
Control of Respiration: Medullary Respiratory Centers
Figure 22.24
Control of Respiration: Pons Respiratory Centers
Pons centers:
Influence and modify activity of the medullary centers
Smooth out inspiration and expiration transitions and vice versa
The pontine respiratory group (PRG) continuously inhibits the inspiration center
Respiratory Rhythm
A result of reciprocal inhibition of the interconnected neuronal networks in the medulla Other theories include
Inspiratory neurons are pacemakers and have intrinsic automaticity and rhythmicity
Stretch receptors in the lungs establish respiratory rhythm
Depth and Rate of Breathing
Inspiratory depth is determined by how actively the respiratory center stimulates the respiratory muscles
Rate of respiration is determined by how long the inspiratory center is active Respiratory centers in the pons and medulla are sensitive to both excitatory and inhibitory stimuli
Medullary Respiratory Centers
Figure 22.25
Depth and Rate of Breathing: Reflexes
Pulmonary irritant reflexes irritants promote reflexive constriction of air passages Inflation reflex (Hering-Breuer) stretch receptors in the lungs are stimulated by lung inflation Upon inflation, inhibitory signals are sent to the medullary inspiration center to end inhalation and allow expiration
Depth and Rate of Breathing: Higher Brain Centers
Hypothalamic controls act through the limbic system to modify rate and depth of respiration
Example: breath holding that occurs in anger
A rise in body temperature acts to increase respiratory rate
Cortical controls are direct signals from the cerebral motor cortex that bypass medullary controls
Examples: voluntary breath holding, taking a deep breath
Depth and Rate of Breathing: PCO2
Changing PCO2 levels are monitored by chemoreceptors of the brain stem
Carbon dioxide in the blood diffuses into the cerebrospinal fluid where it is hydrated Resulting carbonic acid dissociates, releasing hydrogen ions PCO2 levels rise (hypercapnia) resulting in increased depth and rate of breathing
Depth and Rate of Breathing: PCO2
Figure 22.26
Depth and Rate of Breathing: PCO2
Hyperventilation increased depth and rate of breathing that:
Quickly flushes carbon dioxide from the blood
Occurs in response to hypercapnia
Though a rise CO2 acts as the original stimulus, control of breathing at rest is regulated by the hydrogen ion concentration in the brain
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
Depth and Rate of Breathing: PCO2
Arterial oxygen levels are monitored by the aortic and carotid bodies Substantial drops in arterial PO2 (to 60 mm Hg) are needed before oxygen levels become a major stimulus for increased ventilation If carbon dioxide is not removed (e.g., as in emphysema and chronic bronchitis), chemoreceptors become unresponsive to PCO2 chemical stimuli In such cases, PO2 levels become the principal respiratory stimulus (hypoxic drive)
Depth and Rate of Breathing: Arterial pH
Changes in arterial pH can modify respiratory rate even if carbon dioxide and oxygen levels are normal Increased ventilation in response to falling pH is mediated by peripheral chemoreceptors
Peripheral Chemoreceptors
Figure 22.27
Depth and Rate of Breathing: Arterial pH
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
Ventilation and work
Increased work is initially matched by increased ventilation At low work rates, extra ventilation achieved largely by increased tidal volume As work continues to increase, breathing rate begins to increase, and tidal volume increases more. At the ventilatory break point, ventilation increases disproportionately to work.
Respiratory Adjustments: Exercise
Respiratory adjustments are geared to both the intensity and duration of exercise
During vigorous exercise:
Ventilation can increase 20 fold
Breathing becomes deeper and more vigorous, but respiratory rate may not be significantly changed (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
Respiratory Adjustments: Exercise
As exercise begins:
Ventilation increases abruptly, rises slowly, and reaches a steady state
When exercise stops:
Ventilation declines suddenly, then gradually decreases to normal
Ventilation during exercise
Respiratory Adjustments: Exercise
Neural factors bring about the above changes, including:
Psychic stimuli
Cortical motor activation
Excitatory impulses from proprioceptors in muscles
Respiratory Adjustments: High Altitude
The body responds to quick movement to high altitude (above 8000 ft) with symptoms of acute mountain sickness headache, shortness of breath, nausea, and dizziness
Respiratory Adjustments: High Altitude
Acclimatization respiratory and hematopoietic adjustments to altitude include:
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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