22-1 Chapter 22 Lecture Outline See PowerPoint Image Slides for all figures and tables pre-inserted...

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22-1 Chapter 22 Lecture Outline See PowerPoint Image Slides for all figures and tables pre- inserted into PowerPoint without notes. Copyright (c) The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

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22-1

Chapter 22

Lecture Outline

See PowerPoint Image Slides

for all figures and tables pre-inserted into

PowerPoint without notes.

Copyright (c) The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

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22-2

Respiratory System

• Anatomy of the Respiratory System

• Pulmonary Ventilation

• Gas Exchange and Transport

• Respiratory Disorders

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22-3

General Aspects

• Airflow in lungs– bronchi bronchioles alveoli

• Conducting division– passages for airflow, nostrils to bronchioles

• Respiratory division– distal gas-exchange regions, alveoli

• Upper respiratory tract– organs in head and neck, nose through larynx

• Lower respiratory tract– organs of thorax, trachea through lungs

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22-4

Alveolar Blood Supply

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22-5

Alveolus

Fig. 22.11

b and c

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22-6

Pleurae and Pleural Fluid

• Visceral (on lungs) and parietal (lines rib cage) pleurae

• Pleural cavity - space between pleurae, lubricated with fluid

• Functions– reduce friction– create pressure gradient

• lower pressure assists lung inflation

– compartmentalization• prevents spread of infection

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22-7

Pulmonary Ventilation

• Breathing (pulmonary ventilation) – one cycle of inspiration and expiration (respiratory cycle)– quiet respiration – at rest– forced respiration – during exercise

• Flow of air in and out of lung requires a pressure difference between air pressure within lungs and outside body

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22-8

Respiratory Muscles• Diaphragm (dome shaped)

– contraction flattens diaphragm

• Scalenes - hold first pair of ribs stationary

• External and internal intercostals– stiffen thoracic cage; increases diameter

• Pectoralis minor, sternocleidomastoid and erector spinae muscles– used in forced inspiration

• Abdominals and latissimus dorsi– forced expiration (to sing, cough, sneeze)

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22-9

Respiratory Muscles

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22-10

Neural Control of Breathing

• Breathing depends on repetitive stimuli from brain

• Neurons in medulla oblongata and pons control unconscious breathing

• Voluntary control provided by motor cortex• Inspiratory neurons: fire during inspiration• Expiratory neurons: fire during forced expiration• Fibers of phrenic nerve go to diaphragm;

intercostal nerves to intercostal muscles

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22-11

Respiratory Control Centers• Respiratory nuclei in medulla

– Ventral Respiratory Group- primary generator of the respiratory rhythm

– Inspiratory neurons and expiratory neurons, p 877, 878– Dorsal Respiratory Group, integrating center that

receives input from other areas (pons, cehmosensitive area in medulla, peripheral chemoreceptors, and stretch and irritant receptors

• Pons– Pontine respiratory group– Receives input from higher brain centers and

transmits signals to VRG and DRG that modify timing of transition from inspiration to expiration

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22-12

Respiratory Control Centers

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22-13

Input to Respiratory Centers

• From limbic system and hypothalamus– respiratory effects of pain and emotion

• From airways and lungs– irritant receptors in respiratory mucosa

• stimulate vagal afferents to medulla, results in bronchoconstriction or coughing

– stretch receptors in airways - inflation reflex• excessive inflation triggers reflex• stops inspiration

• From chemoreceptors– monitor blood pH, CO2 and O2 levels

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22-14

Chemoreceptors

• Peripheral chemoreceptors – found in major blood vessels

• aortic bodies – signals medulla by vagus nerves

• carotid bodies – signals medulla by glossopharyngeal nerves

• Central chemoreceptors – in medulla

• primarily monitor pH of CSF

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22-15

Peripheral Chemoreceptor Paths

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22-16

Voluntary Control

• Neural pathways– motor cortex of frontal lobe of cerebrum sends

impulses down corticospinal tracts to respiratory neurons in spinal cord, bypassing brainstem

• Limitations on voluntary control– blood CO2 and O2 limits cause automatic

respiration

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22-17

Pressure and Flow

• Atmospheric pressure drives respiration– 1 atmosphere (atm) = 760 mmHg

• Intrapulmonary pressure and lung volume

Boyle’s Law: pressure is inversely proportional to volume

• for a given amount of gas, as volume , pressure and as volume , pressure

• Pressure gradients– difference between atmospheric and

intrapulmonary pressure– created by changes in volume thoracic cavity

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Inspiration

Put your hands on your rib cage. Inhale. Notice that the thoracic cage moves up and out. Diaphragm moves down (Fig 22-8, A and C Herlihy)

• This movement increases the volume of the thoracic cavity and lungs.

• As the volume in the lung increases, the pressure in the lung decreases (Boyle’s Law)

• P in the lung < atmospheric P so air flows in 22-18

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22-19

Respiratory Cycle

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22-20

Passive Expiration

• During quiet breathing, expiration achieved by elasticity of lungs and thoracic cage

• Diaphragm relaxes, moves up. Rib cage moves down and in.

• As volume of thoracic cavity , intrapulmonary pressure and air is expelled

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22-21

Forced Expiration

• Internal intercostal muscles – depress the ribs

• Contract abdominal muscles intra-abdominal pressure forces

diaphragm upward pressure on thoracic cavity

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22-22

Pneumothorax

• Presence of air in pleural cavity– loss of negative intrapleural pressure allows

lungs to recoil and collapse

• Collapse of lung (or part of lung) is called atelectasis

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22-23

Resistance to Airflowthe greater the resistance, the slower the flow

• Pulmonary compliance– The ease with which the lungs expand– change in lung volume relative to a change in

transpulmonary pressure

• Bronchiolar diameter– primary control over resistance to airflow– Bronchoconstriction (reduce airflow)

• triggered by airborne irritants, cold air, parasympathetic stimulation, histamine

– Bronchodilation (increase airflow)• sympathetic nerves, epinephrine

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22-24

Alveolar Surface Tension

• Thin film of water needed for gas exchange– creates surface tension that acts to collapse

alveoli and distal bronchioles

• Pulmonary surfactant (great alveolar cells)

– decreases surface tension

• Premature infants that lack surfactant suffer from respiratory distress syndrome

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22-25

Alveolar Ventilation• Dead air

– fills conducting division of airway, cannot exchange gases

• Anatomic dead space– conducting division of airway

• Physiologic dead space– sum of anatomic dead space and any

pathological alveolar dead space

• Alveolar ventilation rate– air that ventilates alveoli X respiratory rate– directly relevant to ability to exchange gases

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22-26

Measurements of Ventilation

• Spirometer - measures ventilation

• Respiratory volumes– tidal volume: volume of air in one quiet breath– inspiratory reserve volume

• air in excess of tidal inspiration that can be inhaled with maximum effort

– expiratory reserve volume• air in excess of tidal expiration that can be exhaled

with maximum effort

– residual volume (keeps alveoli inflated)

• air remaining in lungs after maximum expiration

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22-27

Lung Volumes and Capacities

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22-28

• Vital capacity– total amount of air that can be exhaled with

effort after maximum inspiration• assesses strength of thoracic muscles and

pulmonary function

• Inspiratory capacity– maximum amount of air that can be inhaled

after a normal tidal expiration

• Functional residual capacity– amount of air in lungs after a normal tidal

expiration

Respiratory Capacities

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22-29

Respiratory Capacities

• Total lung capacity– maximum amount of air lungs can hold

• Forced expiratory volume (FEV)– % of vital capacity exhaled/ time– healthy adult - 75 to 85% in 1 sec

• Peak flow– maximum speed of exhalation

• Minute respiratory volume (MRV)– TV x respiratory rate, at rest 500 x 12 = 6 L/min– maximum: 125 to 170 L/min

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22-30

Respiratory Volumes and Capacities

• Age - lung compliance, respiratory muscles weaken

• Restrictive disorders compliance and vital capacity (limit amt

lungs can be inflated)

• Obstructive disorders– interfere with airflow by narrowing or blocking

the airway

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22-31

Composition of Air• Dalton’s Law: total atmospheric pressure is a sum of the

contributions of the individual gases

• Mixture of gases; each contributes its partial pressure– at sea level 1 atm. of pressure = 760 mmHg– nitrogen constitutes 78.6% of the atmosphere so

• PN2 = 78.6% x 760 mmHg = 597 mmHg

• PO2 = 159

• PH2O = 3.7

• PCO2 = + 0.3

• PN2 + PO

2 + PH2O + PCO

2 = 760 mmHg

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22-32

Composition of Air

• Partial pressures (as well as solubility of gas)

– determine rate of diffusion of each gas and gas exchange between blood and alveolus

• Alveolar air– humidified, exchanges gases with blood, mixes with

residual air – contains:

• PN2 = 569

• PO2 = 104

• PH2O = 47

• PCO2 = 40 mmHg

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22-33

Air-Water Interface

• Important for gas exchange between air in lungs and blood in capillaries

• Gases diffuse down their concentration gradients

• Henry’s law– amount of gas that dissolves in water is

determined by its solubility in water and its partial pressure in air

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22-34

Alveolar Gas Exchange

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22-35

Alveolar Gas Exchange

• Time required for gases to equilibrate = 0.25 sec

• RBC transit time at rest = 0.75 sec to pass through alveolar capillary

• RBC transit time with vigorous exercise = 0.3 sec

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22-36

Factors Affecting Gas Exchange• Concentration gradients of gases

– PO2 = 104 in alveolar air versus 40 in blood

– PCO2 = 46 in blood arriving versus 40 in alveolar

air

• Gas solubility– CO2 20 times as soluble as O2

• O2 has conc. gradient, CO2 has solubility

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22-37

Factors Affecting Gas Exchange• Membrane thickness - only 0.5 m thick

• Membrane surface area - 100 ml blood in alveolar capillaries, spread over 70 m2

• Ventilation-perfusion coupling - areas of good ventilation need good perfusion (vasodilation)

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22-38

Concentration Gradients of Gases

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22-39

Ambient Pressure and Concentration Gradients

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22-40

Lung Disease Affects Gas Exchange

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22-41

Perfusion Adjustments

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22-42

Ventilation Adjustments

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22-43

Oxygen Transport

• Concentration in arterial blood– 20 ml/dl

• 98.5% bound to hemoglobin• 1.5% dissolved

• Binding to hemoglobin– each heme group of 4 globin chains may

bind O2

– oxyhemoglobin (HbO2 )

– deoxyhemoglobin (HHb)

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22-44

Oxygen Transport

• Oxyhemoglobin dissociation curve– relationship between hemoglobin saturation

and PO2 is not a simple linear one

– after binding with O2, hemoglobin changes

shape to facilitate further uptake (positive

feedback cycle)

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22-45

Oxyhemoglobin Dissociation Curve

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22-46

Carbon Dioxide Transport

• As carbonic acid - 90%– CO2 + H2O H2CO3 HCO3

- + H+

• As carbaminohemoglobin (HbCO2)- 5% binds to amino groups of Hb (and plasma proteins)

• As dissolved gas - 5%

• Alveolar exchange of CO2

– carbonic acid - 70% – carbaminohemoglobin - 23%– dissolved gas - 7%

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22-47

Systemic Gas Exchange• CO2 loading

– carbonic anhydrase in RBC catalyzes• CO2 + H2O H2CO3 HCO3

- + H+

– chloride shift• keeps reaction proceeding, exchanges HCO3

-

for Cl- (H+ binds to hemoglobin)

• O2 unloading– H+ binding to HbO2 its affinity for O2

• Hb arrives 97% saturated, leaves 75% saturated - venous reserve

– utilization coefficient • amount of oxygen Hb has released 22%

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22-48

Systemic Gas Exchange

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22-49

Alveolar Gas Exchange Revisited

• Reactions are reverse of systemic gas exchange

• CO2 unloading

– as Hb loads O2 its affinity for H+ decreases, H+ dissociates from Hb and bind with HCO3

-

• CO2 + H2O H2CO3 HCO3- + H+

– reverse chloride shift

• HCO3- diffuses back into RBC in exchange

for Cl-, free CO2 generated diffuses into alveolus to be exhaled

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22-50

Alveolar Gas Exchange

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22-51

Factors Affect O2 Unloading

• Active tissues need oxygen!

– ambient PO2: active tissue has PO

2 ; O2 is

released

– temperature: active tissue has temp; O2 is

released

– Bohr effect: active tissue has CO2, which

lowers pH O2 is released

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22-52

Oxygen Dissociation and Temperature

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22-53

Oxygen Dissociation and pH

Bohr effect: release of O2 in response to low pH

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22-54

• Haldane effect– low level of HbO2 (as in active tissue) enables

blood to transport more CO2

– HbO2 does not bind CO2 as well as deoxyhemoglobin (HHb)

– HHb binds more H+ than HbO2

• as H+ is removed this shifts the

CO2 + H2O HCO3- + H+

reaction to the right

Factors Affecting CO2 Loading

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22-55

Blood Chemistry and Respiratory Rhythm

• Rate and depth of breathing adjusted to maintain levels of:– pH

– PCO2

– PO2

• Let’s look at their effects on respiration:

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22-56

Effects of Hydrogen Ions

• pH of CSF (most powerful respiratory stimulus)

• Respiratory acidosis (pH < 7.35) caused by failure of pulmonary ventilation

– hypercapnia: PCO2 > 43 mmHg

• CO2 easily crosses blood-brain barrier

• in CSF the CO2 reacts with water and releases H+

• central chemoreceptors strongly stimulate inspiratory center

– “blowing off ” CO2 pushes reaction to the left CO2 (expired) + H2O H2CO3 HCO3

- + H+

– so hyperventilation reduces H+ (reduces acid)

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22-57

Effects of Hydrogen Ions

• Respiratory alkalosis (pH > 7.45)

– hypocapnia: PCO2 < 37 mmHg

– Hypoventilation ( CO2), pushes reaction to the right CO2 + H2O H2CO3 HCO3

- + H+

H+ (increases acid), lowers pH to normal

• pH imbalances can have metabolic causes– uncontrolled diabetes mellitus

• fat oxidation causes ketoacidosis, may be compensated for by Kussmaul respiration

(deep rapid breathing)

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22-58

Effects of Carbon Dioxide

• Indirect effects on respiration– through pH as seen previously

• Direct effects CO2 may directly stimulate peripheral

chemoreceptors and trigger ventilation more quickly than central chemoreceptors

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22-59

Effects of Oxygen

• Usually little effect

• Chronic hypoxemia, PO2 < 60 mmHg,

can significantly stimulate ventilation– emphysema, pneumonia– high altitudes after several days

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22-60

Hypoxia

• Causes:– hypoxemic hypoxia - usually due to inadequate

pulmonary gas exchange• high altitudes, drowning, aspiration, respiratory

arrest, degenerative lung diseases, CO poisoning

– ischemic hypoxia - inadequate circulation– anemic hypoxia - anemia– histotoxic hypoxia - metabolic poison (cyanide)

• Signs: cyanosis - blueness of skin

• Primary effect: tissue necrosis, organs with high metabolic demands affected first

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22-61

Oxygen Excess

• Oxygen toxicity: pure O2 breathed at 2.5 atm or greater– generates free radicals and H2O2

– destroys enzymes– damages nervous tissue– leads to seizures, coma, death

• Hyperbaric oxygen– formerly used to treat premature infants,

caused retinal damage, discontinued

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22-62

Chronic Obstructive Pulmonary Disease

• Asthma– allergen triggers histamine release– intense bronchoconstriction (blocks air flow)

• Other COPD’s usually associated with smoking

– chronic bronchitis – emphysema

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22-63

Chronic Obstructive Pulmonary Disease

• Chronic bronchitis – cilia immobilized and in number– goblet cells enlarge and produce excess

mucus– sputum formed (mucus and cellular debris)

• ideal growth media for bacteria

– leads to chronic infection and bronchial inflammation

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22-64

Chronic Obstructive Pulmonary Disease

• Emphysema (barrel chest)– alveolar walls break down

• much less respiratory membrane for gas exchange– healthy lungs are like a sponge; in emphysema, lungs are

more like a rigid balloon

– lungs fibrotic and less elastic– air passages collapse

• obstruct outflow of air• air trapped in lungs

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22-65

Effects of COPD

pulmonary compliance and vital capacity

• Hypoxemia, hypercapnia, respiratory acidosis– hypoxemia stimulates erythropoietin release

and leads to polycythemia

• cor pulmonale – hypertrophy and potential failure of right heart

due to obstruction of pulmonary circulation

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22-66

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– dividing cells invade bronchial wall, cause

bleeding lesions– dense swirls of keratin replace functional

respiratory tissue

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22-67

Lung Cancer

• Adenocarcinoma – originates in mucous glands of lamina propria

• Small-cell (oat cell) carcinoma– least common, most dangerous– originates in primary bronchi, invades

mediastinum, metastasizes quickly

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22-68

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

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22-69

Healthy Lung/Smokers Lung- Carcinoma