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Copyright 2009, John Wiley & Sons, Inc. Chapter 23: The Respiratory System

Copyright 2009, John Wiley & Sons, Inc. Chapter 23: The Respiratory System

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Page 1: Copyright 2009, John Wiley & Sons, Inc. Chapter 23: The Respiratory System

Copyright 2009, John Wiley & Sons, Inc.

Chapter 23: The Respiratory

System

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Copyright 2009, John Wiley & Sons, Inc.

Respiratory System Anatomy

Structurally Upper respiratory system

Nose, pharynx and associated structures Lower respiratory system

Larynx, trachea, bronchi and lungs Functionally

Conducting zone – conducts air to lungs Nose, pharynx, larynx, trachea, bronchi, bronchioles and

terminal bronchioles Respiratory zone – main site of gas exchange

Respiratory bronchioles, alveolar ducts, alveolar sacs, and alveoli

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Nose

External nose – portion visible on face Internal nose – large cavity beyond nasal

vestibule Internal nares or choanae Ducts from paranasal sinuses and nasolacrimal

ducts open into internal nose Nasal cavity divided by nasal septum Nasal conchae subdivide cavity into meatuses

Increase surface are and prevents dehydration Olfactory receptors in olfactory epithelium

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Pharynx

Starts at internal nares and extends to cricoid cartilage of larynx

Contraction of skeletal muscles assists in deglutition Functions

Passageway for air and food Resonating chamber Houses tonsils

3 anatomical regions Nasopharynx Oropharynx Laryngopharynx

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Larynx

Short passageway connecting laryngopharynx with trachea Composed of 9 pieces of cartilage

Thyroid cartilage or Adam’s apple Cricoid cartilage hallmark for tracheotomy

Epiglottis closes off glottis during swallowing Glottis – pair of folds of mucous membranes, vocal folds

(true vocal cords and rima glottidis) Cilia in upper respiratory tract move mucous and trapped

particles down toward pharynx Cilia in lower respiratory tract move them up toward

pharynx

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Larynx

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Structures of Voice Production

Mucous membrane of larynx forms Ventricular folds (false vocal cords) – superior pair

Function in holding breath against pressure in thoracic cavity

Vocal folds (true vocal cords) – inferior pair Muscle contraction pulls elastic ligaments which stretch

vocal folds out into airway Vibrate and produce sound with air Folds can move apart or together, elongate or shorten,

tighter or looser Androgens make folds thicker and longer – slower

vibration and lower pitch

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Trachea

Extends from larynx to superior border of T5 Divides into right and left primary bronchi

4 layers Mucosa Submucosa Hyaline cartilage Adventitia

16-20 C-shaped rings of hyaline cartilage Open part faces esophagus

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Location of Trachea

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Bronchi

Superior border of 5th thoracic vertebra trachea divides into right and left primary bronchus.

Right is more vertical, shorter, and wider – aspiration more likely to affect right side

Carina – site where bronchi divide is an internal ridge Most sensitive area for triggering cough reflex

Divide to form bronchial tree Secondary lobar bronchi (one for each lobe), tertiary

(segmental) bronchi, bronchioles, terminal bronchioles

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Bronchi

Structural changes with branching Mucous membrane changes – ciliated simple columnar with

goblet cells in larger bronchioles to ciliated simple cuboidal with no goblet cells in smaller bronchioles to mostly nonciliated simple cuboidal in terminal bronchioles (macrophages take over)

Incomplete rings of cartilage become plates and then disappear in distal bronchioles

As cartilage decreases, smooth muscle increases Sympathetic ANS – relaxation/ dilation Parasympathetic ANS and histamine have opposite effect –

contraction/ constriction

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Lungs

Separated from each other by the heart and other structures in the mediastinum

Each lung enclosed by double-layered pleural membrane Parietal pleura – lines wall of thoracic cavity Visceral pleura – covers lungs themselves

Pleural cavity is space between layers Pleural fluid reduces friction, produces surface tension (stick

together) Cardiac notch – heart makes left lung 10% smaller

than right

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Relationship of the Pleural Membranes to Lungs

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Anatomy of Lungs

Lobes – each lung divides by 1 or 2 fissures Each lobe receives it own secondary (lobar) bronchus

that branch into tertiary (segmental) bronchi Lobules wrapped in elastic connective tissue

and contains a lymphatic vessel, arteriole, venule and branch from terminal bronchiole

Terminal bronchioles branch into respiratory bronchioles which divide into alveolar ducts

About 25 orders of branching

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Microscopic Anatomy of Lobule of Lungs

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Alveoli

Cup-shaped outpouching Alveolar sac – 2 or more alveoli sharing a

common opening 2 types of alveolar epithelial cells

Type I alveolar cells – form nearly continuous lining, more numerous than type II, main site of gas exchange

Type II alveolar cells – free surfaces contain microvilli, secrete alveolar fluid (surfactant reduces tendency to collapse)

Surfactant - a combination of phospholipids and lipoproteins that reduce surface tension preventing alveoli from collapsing

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Alveolus

Respiratory membrane Alveolar wall – type I and type II alveolar cells Epithelial basement membrane Capillary basement membrane Capillary endothelium Very thin – only 0.5 µm thick to allow rapid diffusion of

gases Lungs receive blood from

Pulmonary artery – “deoxygenated” blood Bronchial arteries – oxygenated blood to perfuse

muscular walls of bronchi and bronchioles

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Components of Alveolus

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Pulmonary ventilation

Respiration (gas exchange) steps1. Pulmonary ventilation/ breathing

Inhalation and exhalation Exchange of air between atmosphere and alveoli

2. External (pulmonary) respiration Exchange of gases between alveoli and blood

3. Internal (tissue) respiration Exchange of gases between systemic capillaries and

tissue cells Supplies cellular respiration (makes ATP)

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Inhalation/ inspiration

Pressure inside alveoli must become lower than atmospheric pressure for air to flow into lungs 760 millimeters of mercury (mmHg) or 1

atmosphere (1 atm) Achieved by increasing size of lungs

Boyle’s Law – pressure of a gas in a closed container is inversely proportional to the volume of the container

Inhalation – lungs must expand, increasing lung volume, decreasing pressure below atmospheric pressure

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Boyle’s Law

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Inhalation

Inhalation is active – Contraction of Diaphragm – most important muscle of inhalation

Flattens, lowering dome when contracted Responsible for 75% of air entering lungs during normal quiet

breathing External intercostals

Contraction elevates ribs 25% of air entering lungs during normal quiet breathing

Accessory muscles for deep, forceful inhalation When thorax expands, parietal and visceral pleurae adhere

tightly due to subatmospheric pressure and surface tension – pulled along with expanding thorax

As lung volume increases, alveolar (intrapulmonic) pressure drops

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Exhalation/ expiration

Pressure in lungs greater than atmospheric pressure Normally passive – muscle relax instead of contract

Based on elastic recoil of chest wall and lungs from elastic fibers and surface tension of alveolar fluid

Diaphragm relaxes and become dome shaped External intercostals relax and ribs drop down

Exhalation only active during forceful breathing

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Airflow

Air pressure differences drive airflow 3 other factors affect rate of airflow and ease of

pulmonary ventilation Surface tension of alveolar fluid

Causes alveoli to assume smallest possible diameter Accounts for 2/3 of lung elastic recoil Prevents collapse of alveoli at exhalation

Lung compliance High compliance means lungs and chest wall expand easily Related to elasticity and surface tension

Airway resistance Larger diameter airway has less resistance Regulated by diameter of bronchioles & smooth muscle tone

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Lung volumes and capacities

The minute volume of respiration is the total volume of air taken in during one minute

tidal volume x 12 respirations per minute = 6000 ml/min

Tidal volume is normally 500 mL Does not account for dead space

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Lung Volumes

Only about 70% of tidal volume reaches respiratory zone

Other 30% remains in conducting zone Anatomic (respiratory) dead space – conducting

airways with air that does not undergo respiratory gas exchange

Alveolar ventilation rate – volume of air per minute that actually reaches respiratory zone

Inspiratory reserve volume – taking a very deep breath

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Spirogram of Lung Volumes and Capacities

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LUNG VOLUMES AND CAPACITIES

Air volumes exchanged during breathing and rate of ventilation are measured with a spiromometer and the record is called a spirogram

Among the pulmonary air volumes exchanged in ventilation are tidal (500 ml) inspiratory reserve (3100 ml) expiratory reserve (1200 ml) residual (1200 ml) minimal volumes.

Only about 350 ml of the tidal volume actually reaches the alveoli, the other 150 ml remains in the airways as anatomic dead space

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LUNG VOLUMES AND CAPACITIES Pulmonary lung capacities, the sum of two

or more volumes, include inspiratory (3600 ml) functional residual (2400 ml) vital (4800 ml) total lung (6000 ml) capacities .

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RESPIRATORY VOLUMES

Tidal volume: During normal breathing about 500mL of air moves into and out of the lungs with each breath.

The amount of air that can be inspired forcibly beyond the tidal volume is called inspiratory reserve volume (IRV).

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RESPIRATORY VOLUMES

Expiratory reserve volume (ERV) is the amount of air that can be evacuated from the lungs after tidal expiration.

Even after the most strenuous expiration only about 1200 mL of air remains in the lungs; this is the residual volume which helps to keep the alveoli patent and prevent lung collapse.

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RESPIRATORY CAPACITIES The inspiratory capacity is the total

amount of air that can be inspired after a tidal expiration, so it is the sum of the TV + IRV.

Functional residual capacity represents the amount of air remaining in the lungs after a tidal expiration and the combined RV + ERV.

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RESPIRATORY CAPACITIES Vital capacity is the total amount of

exchangeable air. It is the sum of TV + IRV + ERV. In healthy young males VC is approximately 4800 mL

Total Lung Capacity is the sum of all lung volumes and is normally around 6 L.

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Dead Space

some of the inspired air fills the conducting passageways and never contributes to gas exchange.

The volume of these conducting zones makes up the anatomic dead space.

Anatomic dead space equals a mL / # of ideal body weight.

This means that in an normal 500 mL TV, only 350 ml is involved in alveolar ventilation.

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PULMONARY FUNCTION TESTS

For evaluating losses in respiratory function and for following the course of certain respiratory diseases.

It cannot provide a specific diagnosis, but it can distinguish between:

obstructive pulmonary disease involving increased airway resistance such as emphysema

restrictive pulmonary diseases involving a reduction in total lung capacity resulting from structural or functional changes in the lungs (TB, fibrosis due to occupational exposure).

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PULMONARY FUNCTION TESTS

More information can be obtained about a patient’s ventilation status by assessing the rate at which gas moves into and out of the lungs.

the minute ventilation is the total amount of gas that flows into or out of the respiratory tract in 1 minute.

During normal quiet breathing the minute ventilation in healthy people is about 6 L/min.

During rigorous exercise the minute ventilation may reach 200 L/min.

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PULMONARY FUNCTION TESTS Two unusual tests are FVC and FEV. FVC, forced vital capacity, measures the amount of gas

expelled when a subject takes a deep breath and the forcefully exhales maximally and as rapidly as possible.

FEV, forced expiratory volume, determines the amount of air expelled during specific time intervals. The volume exhaled during the first second is the FEV1.

Those with healthy lungs can exhale out 80%. Those with obstructive disease exhale considerably less

while those with restrictive disease exhales 80% or more even though their FVC is reduced.

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PULMONARY FUNCTION TESTS Increases in TLC, FRC and RV may occur

due to hyperinflation due to obstructive diseases.

VC, TLC, FRC, and RV are reduced in restrictive diseases with limit lung expansion.

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Exchange of Oxygen and Carbon Dioxide Dalton’s Law

Each gas in a mixture of gases exerts its own pressure as if no other gases were present

Pressure of a specific gas is partial pressure Px

Total pressure is the sum of all the partial pressures Atmospheric pressure (760 mmHg) = PN2 + PO2 + PH2O

+ PCO2 + Pother gases

Each gas diffuses across a permeable membrane from the area where its partial pressure is greater to the area where its partial pressure is less

The greater the difference, the faster the rate of diffusion

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Partial Pressures of Gases in Inhaled AirPN2 =0.786 x 760mm Hg = 597.4 mmHg

PO2 =0.209 x 760mm Hg = 158.8 mmHg

PH2O =0.004 x 760mm Hg = 3.0 mmHg

PCO2 =0.0004 x 760mm Hg = 0.3 mmHg

Pother gases =0.0006 x 760mm Hg = 0.5 mmHg

TOTAL = 760.0 mmHg

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Henry’s law

Quantity of a gas that will dissolve in a liquid is proportional to the partial pressures of the gas and its solubility

Higher partial pressure of a gas over a liquid and higher solubility, more of the gas will stay in solution

Much more CO2 is dissolved in blood than O2 because CO2 is 24 times more soluble

Even though the air we breathe is mostly N2, very little dissolves in blood due to low solubility Decompression sickness (bends)

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External Respiration in Lungs Oxygen

Oxygen diffuses from alveolar air (PO2 105 mmHg) into blood of pulmonary capillaries (PO2 40 mmHg)

Diffusion continues until PO2 of pulmonary capillary blood matches PO2 of alveolar air

Small amount of mixing with blood from conducting portion of respiratory system drops PO2 of blood in pulmonary veins to 100 mmHg

Carbon dioxide Carbon dioxide diffuses from deoxygenated blood in pulmonary

capillaries (PCO2 45 mmHg) into alveolar air (PCO2 40 mmHg) Continues until of PCO2 blood reaches 40 mmHg

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Internal Respiration

Internal respiration – in tissues throughout body Oxygen

Oxygen diffuses from systemic capillary blood (PO2 100 mmHg) into tissue cells (PO2 40 mmHg) – cells constantly use oxygen to make ATP

Blood drops to 40 mmHg by the time blood exits the systemic capillaries

Carbon dioxide Carbon dioxide diffuses from tissue cells (PCO2 45 mmHg) into

systemic capillaries (PCO2 40 mmHg) – cells constantly make carbon dioxide

PCO2 blood reaches 45 mmHg At rest, only about 25% of the available oxygen is used

Deoxygenated blood would retain 75% of its oxygen capacity

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Rate of Pulmonary and Systemic Gas Exchange Depends on

Partial pressures of gases Alveolar PO2 must be higher than blood PO2 for diffusion to

occur – problem with increasing altitude Surface area available for gas exchange Diffusion distance Molecular weight and solubility of gases

O2 has a lower molecular weight and should diffuse faster than CO2 except for its low solubility - when diffusion is slow, hypoxia occurs before hypercapnia

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Transport of Oxygen and Carbon Dioxide Oxygen transport

Only about 1.5% dissolved in plasma 98.5% bound to hemoglobin in red blood cells

Heme portion of hemoglobin contains 4 iron atoms – each can bind one O2 molecule - Oxyhemoglobin

Only dissolved portion can diffuse out of blood into cells

Oxygen must be able to bind and dissociate from heme

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Relationship between Hemoglobin and Oxygen Partial Pressure Higher the PO2, More O2 combines with Hb

Fully saturated – completely converted to oxyhemoglobin Percent saturation expresses average saturation of

hemoglobin with oxygen Oxygen-hemoglobin dissociation curve

In pulmonary capillaries, O2 loads onto Hb In tissues, O2 is not held and unloaded

75% may still remain in deoxygenated blood (reserve)

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Oxygen-hemoglobin Dissociation Curve

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Hemoglobin and Oxygen

Other factors affecting affinity of Hemoglobin for oxygen

Each makes sense if you keep in mind that metabolically active tissues need O2, and produce acids, CO2, and heat as wastes Acidity PCO2

Temperature

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Bohr Effect As acidity increases (pH

decreases), affinity of Hb for O2 decreases

Increasing acidity enhances unloading

Shifts curve to right PCO2

Also shifts curve to right

As PCO2 rises, Hb unloads oxygen more easily

Low blood pH can result from high PCO2

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Temperature Changes

Within limits, as temperature increases, more oxygen is released from Hb

During hypothermia, more oxygen remains bound

2,3-bisphosphoglycerate BPG formed by red

blood cells during glycolysis

Helps unload oxygen by binding with Hb

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Fetal and Maternal Hemoglobin Fetal hemoglobin has a higher affinity for

oxygen than adult hemoglobin Hb-F can carry up to 30% more oxygen Maternal blood’s oxygen readily transferred to fetal

blood

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Carbon Dioxide Transport

Dissolved CO2

Smallest amount, about 7% Carbamino compounds

About 23% combines with amino acids including those in Hb Carbaminohemoglobin

Bicarbonate ions 70% transported in plasma as HCO3

-

Enzyme carbonic anhydrase forms carbonic acid (H2CO3) which dissociates into H+ and HCO3

-

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Chloride shift HCO3

- accumulates inside RBCs as they pick up carbon dioxide

Some diffuses out into plasma To balance the loss of negative ions, chloride (Cl-)

moves into RBCs from plasma Reverse happens in lungs – Cl- moves out as

moves back into RBCs

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-

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CONTROL OF RESPIRATION The area of the brain from which nerve

impulses are sent to respiratory muscles is located bilaterally in the reticular formation of the brain stem.

This respiratory center consists of a medullary rhythmicity area (inspiratory and expiratory areas), pneumotaxic area, and apneustic area (Figure 23.24).

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Medullary Rhythmicity Area

The function of the medullary rhythmicity area is to control the basic rhythm of respiration.

The inspiratory area has an intrinsic excitability of autorhythmic neurons that sets the basic rhythm of respiration.

The expiratory area neurons remain inactive during most quiet respiration but are probably activated during high levels of ventilation to cause contraction of muscles used in forced (labored) expiration (Figure 23.25).

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Pneumotaxic Area

The pneumotaxic area in the upper pons helps coordinate the transition between inspiration and expiration (Figure 23.25).

The apneustic area sends impulses to the inspiratory area that activate it and prolong inspiration, inhibiting expiration.

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Regulation of the Respiratory Center Cortical influences allow conscious control of

respiration that may be needed to avoid inhaling noxious gasses or water.

Breath holding is limited by the overriding stimuli of increased [H+] and [CO2].

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Chemoreceptor Regulation of Respiration

Central chemoreceptors (located in the medulla oblongata) and peripheral chemoreceptors (located in the walls of systemic arteries) monitor levels of CO2 and O2 and provide input to the respiratory center (Figure 23.26).

Central chemoreceptors respond to change in H+ concentration or PCO2, or both in cerebrospinal fluid.

Peripheral chemoreceptors respond to changes in H+, PCO2, and PO2 in blood.

A slight increase in PCO2 (and thus H+), a condition called hypercapnia, stimulates central chemoreceptors (Figure 23.27).

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Central chemoreceptors respond to changes in H+ concentration or PCO2, or both in cerebrospinal fluid.

Peripheral chemoreceptors respond to changes in H+, PCO2, and PO2 in blood.

A slight increase in PCO2 (and thus H+), a condition called hypercapnia, stimulates central chemoreceptors (Figure 23.27).

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As a response to increased PCO2, increased H+ and decreased PO2, the inspiratory area is activated and hyperventilation, rapid and deep breathing, occurs

If arterial PCO2 is lower than 40 mm Hg, a condition called hypocapnia, the chemoreceptors are not stimulated and the inspiratory area sets its own pace until CO2 accumulates and PCO2 rises to 40 mm Hg.

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Severe deficiency of O2 depresses activity of the central chemoreceptors and respiratory center.

Hypoxia refers to oxygen deficiency at the tissue level and is classified in several ways

Hypoxic hypoxia is caused by a low PO2 in arterial blood (high altitude, airway obstruction, fluid in lungs).

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In anemic hypoxia, there is too little functioning hemoglobin in the blood (hemorrhage, anemia, carbon monoxide poisoning).

Stagnant hypoxia results from the inability of blood to carry oxygen to tissues fast enough to sustain their needs (heart failure, circulatory shock).

In histotoxic hypoxia, the blood delivers adequate oxygen to the tissues, but the tissues are unable to use it properly (cyanide poisoning).

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Proprioceptors of joints and muscles activate the inspiratory center to increase ventilation prior to exercise induced oxygen need.

The inflation (Hering-Breuer) reflex detects lung expansion with stretch receptors and limits it depending on ventilatory need and prevention of damage.

Other influences include blood pressure, limbic system, temperature, pain, stretching the anal sphincter, and irritation to the respiratory mucosa

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DISORDERS: HOMEOSTATIC IMBALANCES Asthma is characterized by the following: spasms of

smooth muscle in bronchial tubes that result in partial or complete closure of air passageways; inflammation; inflated alveoli; and excess mucus production. A common triggering factor is allergy, but other factors include emotional upset, aspirin, exercise, and breathing cold air or cigarette smoke.

Chronic obstructive pulmonary disease (COPD) is a type of respiratory disorder characterized by chronic and recurrent obstruction of air flow, which increases airway resistance. The principal types of COPD are emphysema and chronic bronchitis.

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DISORDERS: HOMEOSTATIC IMBALANCES Pneumonia is an acute infection of the alveoli.

The most common cause in the pneumococcal bacteria but other microbes may be involved. Treatment involves antibiotics, bronchodilators, oxygen therapy, and chest physiotherapy.

Tuberculosis (TB) is an inflammation of pleurae and lungs produced by the organism Mycobacterium tuberculosis. It is communicable and destroys lung tissue, leaving nonfunctional fibrous tissue behind.

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DISORDERS: HOMEOSTATIC IMBALANCES Cystic fibrosis is an inherited disease of

secretory epithelia that affects the respiratory passageways, pancreas, salivary glands, and sweat glands.

Sudden Infant Death Syndrome is the sudden death of an apparently healthy infant, usually occurring during sleep. The cause is unknown but may be associated with hypoxia, possibly resulting from sleeping position. As such, it is recommended that infants sleep on their backs for the first six months.

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Page 87: Copyright 2009, John Wiley & Sons, Inc. Chapter 23: The Respiratory System

Copyright 2009, John Wiley & Sons, Inc.

End of Chapter 23

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