Respiratory Volumes Tidal volume (TV) – air that moves into and out of the lungs with each breath (approximately 500 ml) Inspiratory reserve volume (IRV)

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 (1000–1200 ml) Residual volume (RV) – air left in the lungs after strenuous expiration (1200 ml); keeps alveoli inflated

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)

Lung Volumes and Capacities
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Maximum possible inspiration 6,000 5,000 Inspiratory reserve volume Inspiratory capacity Vital capacity 4,000 Tidal volume Lung volume (mL) 3,000 Total lung capacity 2,000 Expiratory reserve volume Functional residual capacity 1,000 Maximum voluntary expiration Residual volume

Dead Space: fills airway, doesn’t exchange gases
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 – those that interfere with airflow by narrowing or blocking the airway make it harder to inhale or exhale a given amount of air asthma, chronic bronchitis emphysema combines elements of restrictive and obstructive disorders Restrictive disorders – reduction in total lung capacity from structural or functional lung changes (reduce pulmonary compliance) limit the amount to which the lungs can be inflated any disease that produces pulmonary fibrosis black-lung, tuberculosis Increases in TLC and RV may occur as a result of obstructive disease Reduction in VC, TLC, and RV result from restrictive disease

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 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 Slow, deep breathing increases AVR and rapid, shallow breathing decreases AVR AVR = frequency X (TV – dead space) (ml/min) (breaths/min) (ml/breath)

Nonrespiratory Air Movements
Most result from reflex action Examples include: coughing, sneezing, crying, laughing, hiccupping, and yawning

Basic Properties of Gases: Dalton’s Law of Partial Pressures
Total pressure of a gas mixture is the sum of the partial pressures O2 21% of atmospheric gas 0.21 * 760 = 160 mm Hg N2 79% of atmospheric gas 0.79 * 760 = 600 mm Hg CO2 0.04% of atmospheric gas * 760 = 0.3 mm Hg partial pressure – the separate contribution of each gas in a mixture

Basic Properties of Gases: Henry’s Law
at the air-water interface, for a given temperature, the amount of gas that dissolves in the water is determined by its solubility in water and its partial pressure in air the greater the PO2 in the alveolar air, the more O2 the blood picks up since blood arriving at an alveolus has a higher PCO2 than air, it releases CO2 into the air at the alveolus, the blood is said to unload CO2 and load O2 The amount of gas that will dissolve in a liquid also depends upon its solubility: Carbon dioxide is the most soluble Oxygen is 1/20th as soluble as carbon dioxide Nitrogen is practically insoluble in plasma

Composition of Alveolar Gas
The atmosphere is mostly oxygen and nitrogen, while alveoli contain more carbon dioxide and water vapor These differences result from: air is humidifies by contact with mucous membranes alveolar PH2O is more than 10 times higher than inhaled air freshly inspired air mixes with residual air left from the previous respiratory cycle oxygen is diluted and it is enriched with CO2 alveolar air exchanges O2 and CO2 with the blood PO2 of alveolar air is about 65% that of inspired air PCO2 is more than 130 times higher

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 (perfusion-ventilation coupling) 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

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

Figure 22.17

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Lung Disease Affects Gas Exchange
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. (a) Normal Fluid and blood cells in alveoli Alveolar walls thickened by edema (b) Pneumonia Confluent alveoli Figure 22.21 (c) Emphysema

Oxygenation of Blood Figure 22.18

Ventilation-Perfusion Coupling
Ventilation – the amount of gas reaching the alveoli Perfusion – the blood flow reaching the alveoli Ventilation and perfusion must be tightly regulated for efficient gas exchange Changes in PCO2 in the alveoli cause changes in the diameters of the bronchioles Passageways servicing areas where alveolar carbon dioxide is high dilate to easily remove the CO2 Those serving areas where alveolar carbon dioxide is low constrict

Ventilation-Perfusion Coupling: PO2 for caps
PCO2 in alveoli Reduced alveolar ventilation; excessive perfusion Pulmonary arterioles serving these alveoli constrict Reduced alveolar ventilation; reduced perfusion PO2 PCO2 in alveoli Enhanced alveolar ventilation; inadequate perfusion Pulmonary arterioles serving these alveoli dilate Enhanced alveolar ventilation; enhanced perfusion Figure 22.19

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 one’s 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

Molecular oxygen is carried in the blood:
Oxygen Transport Molecular oxygen is carried in the blood: 98.5% Bound to hemoglobin (Hb) within red blood cells 1.5% 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

Carbon Monoxide Poisoning
carbon monoxide (CO) - competes for the O2 binding sites on the hemoglobin molecule colorless, odorless gas in cigarette smoke, engine exhaust, fumes from furnaces and space heaters carboxyhemoglobin – CO binds to ferrous ion of hemoglobin binds 210 times as tightly as oxygen ties up hemoglobin for a long time non-smokers - less than 1.5% of hemoglobin occupied by CO smokers- 10% in heavy smokers atmospheric concentrations of 0.2% CO is quickly lethal

The rate that hemoglobin binds and releases oxygen is regulated by:
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

Hemoglobin Saturation Curve
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 20 100 O2 unloaded to systemic tissues 80 15 60 10 Percentage O2 saturation of hemoglobin mL O2 /dL of blood 40 5 20 20 40 60 80 100 Systemic tissues Alveoli Figure 22.23 Partial pressure of O2 (PO2) in mm Hg relationship between hemoglobin saturation and PO2

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 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

Adjustment to the Metabolic Needs of Individual Tissues
hemoglobin unloads O2 to match metabolic needs of different states of activity of the tissues four factors that adjust the rate of oxygen unloading ambient PO2 active tissue has  PO2 ; O2 is released from Hb temperature active tissue has  temp; promotes O2 unloading Bohr effect active tissue has  CO2, which lowers pH of blood ; promoting O2 unloading bisphosphoglycerate (BPG) RBCs produce BPG which binds to Hb; O2 is unloaded Haldane effect – rate of CO2 loading is also adjusted to varying needs of the tissues, low level of oxyhemoglobin enables the blood to transport more CO2  body temp (fever), thyroxine, growth hormone, testosterone, and epinephrine all raise BPG and cause O2 unloading  metabolic rate requires  oxygen

Metabolic needs influence Hemoglobin Saturation
Temperature, H+, PCO2, and BPG Modify the structure of hemoglobin and alter its affinity for oxygen bisphosphoglycerate (BPG): binds Hb, produced by RBCs during glycolysis  body temp (fever), thyroxine, growth hormone, testosterone, and epinephrine all raise BPG and cause O2 unloading Increases of these factors: Decrease hemoglobin’s 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 hemoglobin’s 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 In RBCs, carbonic anhydrase reversibly catalyzes the conversion of carbon dioxide and water to carbonic acid CO2 + H2O  H2CO3 H+ HCO3– Carbon dioxide Water Carbonic acid Hydrogen ion Bicarbonate ion

 CO2 or HCO3- tips balance to right: As a consequence, pH drops
+ H2O  H2CO3 H+ HCO3– Carbon dioxide Water Carbonic acid Hydrogen ion Bicarbonate ion CO2 or HCO3- tips balance to right: As a consequence, pH drops CO2 or HCO3- tips balance to left: As a consequence, pH rises This system is the only important ECF buffer Kidneys lower pH by excreting HCO3- Kidneys raise pH by excreting H+

Figure 22.22a

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

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

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 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 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+ Changes in respiratory rate can also: Alter blood pH Provide a fast-acting system to adjust pH when it is disturbed by metabolic factors

acidosis – blood pH lower than 7.35
Hydrogen Ions acidosis – blood pH lower than 7.35 alkalosis – blood pH higher than 7.45 hypocapnia – PCO2 less than 37 mm Hg (normal 37 – 43 mm Hg) most common cause of alkalosis hypercapnia – PCO2 greater than 43 mm Hg most common cause of acidosis

Effects of Hydrogen Ions
respiratory acidosis and respiratory alkalosis – pH imbalances resulting from a mismatch between the rate of pulmonary ventilation and the rate of CO2 production hyperventilation is a corrective homeostatic response to acidosis “blowing off ” CO2 faster than the body produces it pushes reaction to the left CO2 (expired) + H2O  H2CO3  HCO3- +  H+ reduces H+ (reduces acid) raises blood pH towards normal

Effects of Hydrogen Ions
hypoventilation is a corrective homeostatic response to alkalosis allows CO2 to accumulate in the body fluids faster than we exhale it shifts reaction to the right CO2 + H2O  H2CO3  HCO3- + H+ raising the H+ concentration, lowering pH to normal ketoacidosis – acidosis brought about by rapid fat oxidation releasing acidic ketone bodies (diabetes mellitus) induces Kussmaul respiration – hyperventilation cannot remove ketone bodies, but blowing off CO2, it reduces the CO2 concentration and compensates for the ketone bodies to some degree

Control of Respiration: Medullary Respiratory Centers
The ventral respiratory group (VRG), or inspiratory center: Sets basic respiratory rhythm Excites the inspiratory muscles and sets eupnea (12-15 breaths/minute) Becomes dormant during (passive) expiration inspiratory neurons: fire during inspiration expiratory neurons: fire during forced expiration The dorsal respiratory group (DRG) modifies the rate and depth of breathing receives influences from external sources innervation fibers of phrenic nerve supply diaphragm intercostal nerves supply intercostal muscles

Control of Respiration: Pons Respiratory Centers
Pons centers: Influence and modify activity of the medullary centers based on activity (sleep, exercise, talking) modifies rhythm of the VRG by outputs to both the VRG and DRG

Other theories include
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

Central and Peripheral Input to Respiratory Centers
hyperventilation – anxiety triggered state in which breathing is so rapid that it expels CO2 from the body faster than it is produced. As blood CO2 levels drop, the pH rises causing the cerebral arteries to constrict reducing cerebral perfusion which may cause dizziness or fainting can be brought under control by having the person rebreathe the expired CO2 from a paper bag central chemoreceptors – brainstem neurons that respond to changes in pH of cerebrospinal fluid pH of cerebrospinal fluid reflects the CO2 level in the blood by regulating respiration to maintain stable pH, respiratory center also ensures stable CO2 level in the blood peripheral chemoreceptors – located in the carotid and aortic bodies of the large arteries above the heart respond to the O2 and CO2 content and the pH of blood

Central and Peripheral Input to Respiratory Centers
stretch receptors – found in the smooth muscles of bronchi and bronchioles, and in the visceral pleura respond to inflation of the lungs inflation (Hering-Breuer) reflex – triggered by excessive inflation protective reflex that inhibits inspiratory neurons stopping inspiration irritant receptors – nerve endings amid the epithelial cells of the airway respond to smoke, dust, pollen, chemical fumes, cold air, and excess mucus trigger protective reflexes such as bronchoconstriction, shallower breathing, breath-holding (apnea), or coughing

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

Figure 22.26

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 Hypoventilation – slow and shallow breathing due to abnormally low PCO2 levels Apnea (breathing cessation) may occur until PCO2 levels rise

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) 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

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

As exercise begins: Ventilation increases abruptly, rises slowly, and reaches a steady state When exercise stops: Ventilation declines suddenly, then gradually decreases to normal

Neural factors bring about the above changes, including: Psychic stimuli Cortical motor activation Excitatory impulses from proprioceptors in muscles PLAY InterActive Physiology ®: Control of Respiration, pages 3–15

Chronic Obstructive Pulmonary Disease
COPD – refers to any disorder in which there is a long-term obstruction of airflow and a substantial reduction in pulmonary ventilation major COPDs are chronic bronchitis and emphysema usually associated with smoking other risk factors include air pollution or occupational exposure to airborne irritants

chronic bronchitis inflammation and hyperplasia of the bronchial mucosa cilia immobilized and reduced in number goblet cells enlarge and produce excess mucus develop chronic cough to bring up extra mucus with less cilia to move it sputum formed (mucus and cellular debris) ideal growth media for bacteria incapacitates alveolar macrophages leads to chronic infection and bronchial inflammation symptoms include dyspnea, hypoxia, cyanosis, and attacks of coughing

emphysema alveolar walls break down lung has larger but fewer alveoli much less respiratory membrane for gas exchange lungs fibrotic and less elastic healthy lungs are like a sponge; in emphysema, lungs are more like a rigid balloon air passages collapse obstructs outflow of air air trapped in lungs weaken thoracic muscles spend three to four times the amount of energy just to breathe

reduces pulmonary compliance and vital capacity
Effects of COPD reduces pulmonary compliance and vital capacity hypoxemia, hypercapnia, respiratory acidosis hypoxemia stimulates erythropoietin release from kidneys - leads to polycythemia cor pulmonale hypertrophy and potential failure of right heart due to obstruction of pulmonary circulation

Smoking and Lung Cancer
lung cancer accounts for more deaths than any other form of cancer most important cause is smoking (15 carcinogens) squamous-cell carcinoma (most common) begins with transformation of bronchial epithelium into stratified squamous from ciliated pseudostratified epithelium dividing cells invade bronchial wall, cause bleeding lesions dense swirls of keratin replace functional respiratory tissue

small-cell (oat cell) carcinoma
Lung Cancer adenocarcinoma originates in mucous glands of lamina propria small-cell (oat cell) carcinoma least common, most dangerous named for clusters of cells that resemble oat grains originates in primary bronchi, invades mediastinum, metastasizes quickly to other organs

Progression of Lung Cancer
90% originate in primary bronchi tumor invades bronchial wall, compresses airway; may cause atelectasis often first sign is coughing up blood metastasis is rapid; usually occurs by time of diagnosis common sites: pericardium, heart, bones, liver, lymph nodes and brain prognosis poor after diagnosis only 7% of patients survive 5 years

Effect of Smoking Figure 22.27 a-b Tumors
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Tumors (a) Healthy lung, mediastinal surface (b) Smoker's lung with carcinoma a: © The McGraw-Hill Companies/Dennis Strete, photographer; b: Biophoto Associates/Photo Researchers, Inc. Figure a-b

Main Points List the functions of the respiratory system.
Review the structure of the red blood cell and hemoglobin. Identify the location and structure of the organs of respiration. Trace the bronchial tree from the trachea to the alveolus. Compare type I and type II alveoli as to structure, function and numbers. Define “dust” cells. Describe the mechanics of breathing. Explain and compare the respiratory volumes and capacities. Understand the different pressures involved in the mechanics of breathing. Define atelectasis. State Boyle’s Law, Dalton’s Law, and Henry’s Law and relate each to their involvement in respiration. Know the partial pressures of oxygen and carbon dioxide in systemic and pulmonary circulation, as well as at the alveolar and tissue level. Discuss ventilation-perfusion coupling. Describe the effects of pH, temperature, and pCO2 on oxygen unloading. Describe carbon dioxide transport in the blood. Discuss the neural controls of respiration. Define hyperventilation and hypoventilation.

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

Chronic Obstructive Pulmonary Disease (COPD)
Exemplified by chronic bronchitis and obstructive emphysema Patients have a history of: Smoking Dyspnea, where labored breathing occurs and gets progressively worse Coughing and frequent pulmonary infections COPD victims develop respiratory failure accompanied by hypoxemia, carbon dioxide retention, and respiratory acidosis

Pathogenesis of COPD 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

Tuberculosis Infectious disease caused by the bacterium Mycobacterium tuberculosis Symptoms include fever, night sweats, weight loss, a racking cough, and splitting headache Treatment entails a 12-month course of antibiotics

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

Respiratory Acidosis and Alkalosis
Result from failure of the respiratory system to balance pH PCO2 is the single most important indicator of respiratory inadequacy PCO2 levels Normal PCO2 fluctuates between 35 and 45 mm Hg Values above 45 mm Hg signal respiratory acidosis Values below 35 mm Hg indicate respiratory alkalosis

Respiratory Acidosis and Alkalosis
Respiratory acidosis is the most common cause of acid-base imbalance Occurs when a person breathes shallowly (hypoventilation  CO2 retention), or gas exchange is hampered by diseases such as pneumonia, cystic fibrosis, apnea, asthma, or emphysema Respiratory alkalosis is a common result of hyperventilation…emotions, O2 deficiency

Metabolic Acidosis All pH imbalances except those caused by abnormal blood carbon dioxide levels Metabolic acid-base imbalance – bicarbonate ion levels above or below normal (22-26 mEq/L) Metabolic acidosis is the second most common cause of acid-base imbalance Typical causes are ingestion of too much alcohol or aspirin and excessive loss of bicarbonate ions (diarrhea) Other causes include accumulation of lactic acid, shock, ketosis in diabetic crisis, starvation, and kidney failure

Metabolic Alkalosis (rare)
Rising blood pH and bicarbonate levels indicate metabolic alkalosis Typical causes are: Vomiting of the acid contents of the stomach Intake of excess base (e.g., from antacids) Constipation, in which excessive bicarbonate is reabsorbed

Respiratory and Renal Compensations
Acid-base imbalance due to inadequacy of a physiological buffer system is compensated for by the other system The respiratory system will attempt to correct metabolic acid-base imbalances The kidneys will work to correct imbalances caused by respiratory disease

Respiratory Compensation
In metabolic acidosis: The rate and depth of breathing are elevated Blood pH is below 7.35 and bicarbonate level is low As carbon dioxide is eliminated by the respiratory system, PCO2 falls below normal In respiratory acidosis, the respiratory rate is often depressed and is the immediate cause of the acidosis

Respiratory Compensation
In metabolic alkalosis: Compensation exhibits slow, shallow breathing, allowing carbon dioxide to accumulate in the blood Correction is revealed by: High pH (over 7.45) and elevated bicarbonate ion levels Rising PCO2 PLAY InterActive Physiology ®: Acid/Base Homeostasis, page 48–58

Acidosis has high PCO2 and high bicarbonate levels
Renal Compensation To correct respiratory acid-base imbalance, renal mechanisms are stepped up Acidosis has high PCO2 and high bicarbonate levels The high PCO2 is the cause of acidosis The high bicarbonate levels indicate the kidneys are retaining bicarbonate to offset the acidosis

Alkalosis has Low PCO2 and high pH
Renal Compensation Alkalosis has Low PCO2 and high pH The kidneys eliminate bicarbonate from the body by failing to reclaim it or by actively secreting it

Respiratory Volumes Tidal volume (TV) – air that moves into and out of the lungs with each breath (approximately 500 ml) Inspiratory reserve volume (IRV)

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Respiratory Volumes Tidal volume (TV) – air that moves into and out of the lungs with each breath (approximately 500 ml) Inspiratory reserve volume (IRV)

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