The Respiratory - PowerPoint Presentation

Slide1

The Respiratory

SystemSlide2

Function of the

lungs

Ventilation (breathing)

Gas Exchange

T

he movement of oxygen and carbon dioxide between lungs and tissues via blood

Oxygen utilization

The use of oxygen by cells to release energySlide3

The respiratory

acinusCartilage is present to level of proximal bronchioles

Beyond terminal bronchiole gas exchange occurs

The distal airspaces are kept open by elastic tension in alveolar wallsSlide4

Lung Volume

Lungs must stay openAtelectasis = accumulation of pleural fluid which compresses the lung and collapses alveoli

Asthma

= spasm of bronchiolar smooth muscle narrows the airway and constricts air flow

Emphysema

= insufficient respiratory membrane for gas exchange

Interstitial Fibrosis

= an accumulation of fibrous tissue stiffens the lung and prevents free flow of air and also interferes with gas diffusion between blood and alveoliSlide5

Lung Volume

Spirometry

Diagnostic procedure that measures lung volumes and capacities and flow rate of air going into and out of the lungs

Lung Diseases have typical

spirometry patterns

Generalized Diseases come in two categoriesObstructive and Restrictive

Obstructive

= limitation of airflow

Restrictive

= limitation of lung expansionSlide6

Lung Volume

Forced Vital Capacity (FVC)A volume measurement

The amount of air expelled from maximum inspiration to maximum expiration

Patient takes the deepest breath possible and blows out as much as possible, no timing involved

Forced Expiratory Volume (FEV

1

)

Rat measurement; the timed measurement of the amount of air expelled from maximum inspiration in the first second of effect

Patient takes the deepest possible breath and breathes out as hard as possible = amount expelled in first secondSlide7

Lung Volume

FEV1

/FVC = ratio is low in Obstructive disease

Ratio is critical in separating obstructive and restrictive lung disease

In Obstructive disease

The rate of air flowing out of the lungs is slowedThe amount the patient can expel is low

Lung volumes are usually normalSlide8

Lung Volume

Restrictive disease The ratio of airflow to lung volume is usually near normal

Limits both volume and flow rate proportionally

Both Obstructive and Restrictive Disease limits gas exchange

Arterial Oxygen levels are low and Carbon Dioxide levels are highSlide9

Effect of pH on ventilation

Normal level of HCO3- = 24 mEq/L

Metabolic acidosis (HCO

3

- < 24) will + ventilation

Metabolic alkalosis (HCO3- >24) will – ventilation

Kidney regulates HCO

3

-

Normal level of CO

2

= 40 mmHg

Respiratory acidosis (CO

2

> 40) will + ventilation

Respiratory alkalosis (CO

2

< 40) will – ventilation

Lung regulates CO

2

Slide10

Normal Lung TissueSlide11

Static Lung Volumes

Tidal Volume (500ml)amount of air moved in or out each breathInspiratory

Reserve Volume (3000ml)

maximum vol. one can inspire above normal inspiration

Expiratory Reserve Volume (1100ml)

maximum vol. one can expire below normal expirationResidual Volume (1200 ml)

volume of air left in the lungs after maximum expiratory effort Slide12

Static Lung Capacities

Functional residual capacity (RV+ERV)vol. of air left in the lungs after a normal expir

., balance point of lung recoil & chest wall forces

Inspiratory

capacity

(TV+IRV)max. vol. one can inspire during an insp effort

Vital capacity

(IRV+TV+ERV)

max. vol. one can exchange in a resp.

cycle = max exhaled volume

Total lung capacity

(IRV+TV+ERV+RV)

the air in the lungs at full inflationSlide13

Patterns of Breathing

Eupneanormal breathing (12-17 B/min, 500-600 ml/B)

Hyperpnea



pulmonary ventilation matching

 metabolic demand

Hyperventilation

(



CO

2

)



pulmonary ventilation > metabolic demand

Hypoventilation

(



CO

2

)



pulmonary ventilation < metabolic

demand

Hypoperfusion



blood flow to alveoli< metabolic demandSlide14

Patterns of breathing (cont.)

Tachypnea



frequency of respiratory rate

Apnea

Absense of breathing. e.g. Sleep apnea

Dyspnea

Difficult or labored breathing

Orthopnea

Dyspnea

when recumbent, relieved when upright. e.g. congestive heart failure, asthma, lung failureSlide15

General Signs and Symptoms of Respiratory Disease

Hypoxia

: Decreased levels of oxygen in the tissues

Hypoxemia

: Decreased levels of oxygen in arterial blood

Hypercapnia

: Increased levels of CO

2

in the blood

Hypocapnia

: Decreased levels of CO

2

in the blood

Cyanosis

: Bluish discoloration of skin and mucous membranes due to poor oxygenation of the blood

Hemoptysis

: Blood in the sputumSlide16

General Signs and Symptoms of Respiratory Disease

CoughProductive cough

= raising fluid to the pharynx

Expectoration

= spitting

Non-productive cough or hacking

Dyspnea

Shortness of breath

Airway obstruction

Decreased compliance

Cyanosis

Large quantities of

unoxygenated

bloodSlide17

Areas Involved in Respiratory Tract Infections

Upper respiratory tract Nose, sinuses, pharynx, epiglottis, and larynx

Filters, warms, moisturizes and channels air

Lower

respiratory tract

Trachea, bronchi, lungs and pleurae

Oxygenate blood and collects and discharges carbon dioxide, produced by energy metabolismSlide18

Upper respiratory tract Infections

The most common viral pathogens for the “common cold” are

rhinovirus,

parainfluenza

virus, respiratory

syncytial

virus, adenovirus

and

coronavirus

.

These viruses tend to have seasonal variations in their peak incidence.

They gain entry to the body through the nasal mucosa and the surfaces of the eye. They are readily spread from person to person via respiratory secretions.

Manifestations of the common cold include:

Rhinitis:

Inflammation of the nasal mucosa

Sinusitis:

Inflammation of the sinus mucosa

Pharyngitis

:

Inflammation of the pharynx and throat

Headache

Nasal discharge and congestion

The common coldSlide19

Influenza is a viral infection that can affect the upper or lower respiratory tract.

Three distinct forms of influenza virus have been identified: A, B and C, of these three variants, type A is the most common and causes the most serious illness. The influenza virus is a highly transmissible respiratory pathogen.

Because the organism has a high tendency for genetic mutation, new

variants

of the virus are constantly arising in different places around the world. Serious

pandemics (spread of infection across a large region)

of influenza are seen every

8 to 10 years

as a result of this genetic mutation .

Upper respiratory tract Infections

InfluenzaSlide20

Symptoms of influenza infection

: Headache

Fever, chills

Muscle aches

Nasal discharge

Unproductive cough

Sore throat

Influenza infection

can cause

marked inflammation of the respiratory epithelium leading to acute tissue damage and a loss of ciliated cells that protect the respiratory passages from other organisms.

As a result, influenza infection

may lead to

co-infection of the respiratory passages with bacteria.

It is also possible for the influenza virus to infect the tissues of the lung itself to cause a

viral pneumonia

.

Upper respiratory tract Infections

InfluenzaSlide21

Treatment of influenza

:Bed rest, fluids, warmth

Antiviral drugs

Influenza vaccine

:

Provides protection against certain A and B influenza strains that are expected to be prevalent in a certain year.

The vaccine must be updated and administered yearly to be effective but will not be effective against influenza strains not included in the vaccine.

The influenza vaccine is particularly indicated in elderly people, in individuals weakened by other disease and in health-care workers

Influenza

Upper respiratory tract InfectionsSlide22

Drugs for Treating Influenza:

Amantidine

Used orally or by aerosol administration

Effective only against type A influenza

Inhibits viral fusion, assembly and release from the infected host cell

Neuraminidase inhibitors

(

Zanamavir

,

Oseltamivir

)

New drugs that can be used by inhalation (

Zanamavir

) or orally (

Oseltamivir

)

Effective against both type A and B influenza

Inhibits the activity of viral neuraminidase enzyme that is necessary for spread of the influenza virus

Upper respiratory tract Infections

InfluenzaSlide23

Types of Influenza Vaccinations

Trivalent inactivated influenza vaccine

(TIIV)

Developed in the 1940s

Administered by injection

Live, attenuated influenza vaccine

(LAIV)

Approved for use in 2003

Administered

intranasallySlide24

Pneumonia is a condition that involves

inflammation of lower lung structures such as the alveoli or interstitial spaces. It may be

caused by

bacteria or viruses such as

pneumocystis

carinii.

The prevalence and severity of pneumonia have been heightened in recent years due to the emergence of HIV as well as antibiotic resistance.

Pneumonia may be

classified according to

the pathogen that is responsible for the infection.

There tend to be distinct organisms that cause pneumonia in the hospital setting vs. the community setting.

Lower respiratory tract Infections

PneumoniaSlide25

Lower respiratory tract Infections

Pneumonia

Pathology:

Alveolar

Bronchopneumonia (Streptococcus

pneumoniae

,

Haemophilus

influenza, Staphylococcus

aureus

)

Lobar (Streptococcus

pneumoniae

)

Interstitial

(

Influenza virus,

Mycoplasma

pneumoniae

)

Pathogenesis:

Inhalation of air droplets

Aspiration of infected secretions or objects

Hematogenous

spread -

causing infections away from the original site

Slide26

Bronchopneumonia vs. Lobar Pneumonia

BronchopneumoniaAcute Inflammation in the walls of the bronchioles

Lobar Pneumonia

Lobar pneumonia is a form of pneumonia that affects a large and continuous area of the lobe of a lungSlide27
Slide28

Bronchopneumonia

Suppurative

(pus)

inflammation of lung tissue caused by Staph, Strep,

Pneumo

& H. influenza

Usually

bilateral

Lower lobes common, but can occur anywhere

Complications:

Abscess

Empyema

(

is a collection of pus in the space between the lung and the inner surface of the chest wall (pleural space).

DisseminationSlide29

BronchopneumoniaSlide30

BronchopneumoniaSlide31

BronchopneumoniaSlide32
Slide33

Bronchopneumonia:Slide34

BronchopneumoniaSlide35

Individuals Most at Risk for Pneumonia

ElderlyThose with viral infection

Chronically ill

AIDS or

immunosuppressed

patients

Smokers

Patients with chronic respiratory disease e.g. bronchial asthma.

Lower respiratory tract Infections

PneumoniaSlide36

Potential Pathogens

Typical

Streptococcus

pneumoniae

Hemophilus

influenzae

Mycobacterium

catarrhalis

Klebsiella

pneumoniae

Atypical

Chlamydia

pneumoniae

Legionella

pneumophila

Mycoplasma

pneumoniae

.Slide37

Lobar Pneumonia

Fibrinosuppurative consolidation – whole lobe

Rare due to antibiotic treatment.

~95% - Strep

pneumoniae

The course runs in four stages:

Congestion.

Red

Hepatization

– Looks like the liver

Gray

Hepatizaiton

Resolution

Lower respiratory tract Infections

PneumoniaSlide38

Red

hepatisation: (consolidation) describes lung tissue with confluent acute exudation, containing neutrophils and red cells, giving a red, firm, liver-like gross appearance.

Grey

hepatisation

:

follows, as the red cells disintegrate and the remaining fibrinosuppurative

exudate

persists, giving a grey-brown appearance.

Resolution:

is the

favourable

final stage in which consolidated

exudate

undergoes enzymatic and cellular degradation and clearance; normal structure is restored.

Lower respiratory tract Infections

PneumoniaSlide39

Lobar pneumonia

Lobar pneumonia: whole

lobe(s

) involved

grey

hepatizationSlide40

Red

HepatisationSlide41

Red

HepatisationSlide42

Lobar Pneumonia – Gray hep…Slide43

A second classification scheme for pneumonia is based on the

specific structures of the lung that the organisms infect and includes typical and atypical

pneumonia.

Typical pneumonia

• Usually

bacterial

in origin.

• Organisms replicate

in the spaces of the alveoli

.

Manifestations:

• Inflammation and fluid accumulation are seen in the alveoli.

• White cell infiltration and exudation can been seen on chest radiographs.

• High fever, chest pain, chills, and malaise are present.

• Purulent sputum is present.

• Some degree of hypoxemia is present.

Lower respiratory tract Infections

PneumoniaSlide44

Atypical pneumonia

• Usually viral in origin.• Organisms replicate in the spaces around the alveoli.

Manifestations:

•

Milder symptoms than typical pneumonia.

• Lack of white cell infiltration in alveoli.

• Lack of fluid accumulation in the alveoli.

• Not usually evident on radiographs.

• May make the patient susceptible to bacterial pneumonia.

Lower respiratory tract Infections

PneumoniaSlide45

Treatment of pneumonia

:

•

Antibiotics

if bacterial in origin. The health-care provider should consider the possibility that antibiotic-resistant organisms are present.

•

Oxygen

therapy for hypoxemia.

• A

vaccine

for

pneumococcal

pneumonia is currently available and highly effective. This vaccine should be considered in high-risk individuals.

Lower respiratory tract Infections

PneumoniaSlide46

An

abscess is a complication of severe pneumonia, most typically from virulent organisms such as S. aureus

.

Abscesses are complications of aspiration, where they appear more frequently in the right posterior lung.

Lower respiratory tract Infections

AbscessSlide47

Lung Abscess:

Focal suppuration with necrosis of lung

tissue

Organisms commonly cultured:

Staphylococci

Streptococci

Gram-negative

Anaerobes

Frequent mixed infections

Mechanism:

Aspiration

Post pneumonic

Septic embolism

Neoplasms

Productive Cough

, Fever

.

Clubbing

Complications

:

Systemic spread, septicemia.Slide48

ClubbingSlide49

Lung Abscess:Slide50

Abscess formationSlide51

Bronchopneumonia - Abscess formationSlide52

Lung Abscess:Slide53

Caused by

Mycobacterium tuberculosis.Transmitted through inhalation of infected droplets

Primary

Single

granuloma

within parenchyma and

hilar

lymph nodes (

Ghon

complex

).

Infection does not progress (most common).

Progressive primary pneumonia

Miliary

dissemination (blood stream).

Lower respiratory tract Infections

Pulmonary TuberculosisSlide54

Ghon complexSlide55

Forms of Tuberculosis

M. tuberculosis

hominis

(human tuberculosis)

Airborne infection spread by minute droplet nuclei harbored in the respiratory secretions of persons with active tuberculosis

Living under crowded and confined conditions increases the risk for spread of the disease.

Bovine tuberculosis

Acquired by drinking milk from infected cows; initially affects the gastrointestinal tract

Has been virtually eradicated in North America and other developed countriesSlide56

Tuberculosis

GranulomasSlide57

Ghon

ComplexSlide58

Mycobacterium TuberculosisSlide59

Positive Tuberculin Skin Test

Results from a cell-mediated immune response

Implies that a person has been infected with

M. tuberculosis

and has mounted a cell-mediated immune responseDoes not mean the person has active tuberculosisSlide60

IndurationSlide61

Question

Which of the following involves infection of the entire respiratory tract?Common cold

Pneumonia

Tuberculosis

CancerSlide62

Answer

Common cold

Pneumonia: Pneumonia can involve all respiratory tissues and, due to its virulence, is a major health risk.

Tuberculosis

CancerSlide63

Chronic Obstructive Disease

AsthmaChronic Bronchitis

EmphysemaSlide64

Asthma

Extrinsic - response to inhaled antigenIntrinsic - non-immune mechanisms (cold, exercise, aspirin)Slide65

Pathology of asthma

Airway inflammation with mucosal

edema

Mucus pluggingSlide66

Bronchial Asthma

A chronic inflammatory disorder characterised by

hyperreactive

airways leading to

episodic reversible bronchoconstrictionSlide67

Mucosal

edemaSlide68

Mucus plugsSlide69

Mucus plug/inflammationSlide70

Chronic Obstructive Pulmonary Disease

Chronic bronchitisEmphysema

A

smoker’s disease

Due to particulate matter entering the lungsSlide71

Cor

PulmonaleRight heart failure resulting from primary lung disease and long-standing primary or secondary pulmonary hypertension

Involves hypertrophy and the eventual failure of the right ventricle

Manifestations include the signs and symptoms of primary lung disease and the signs of right-sided heart failure.Slide72

COPD

One of the top 5 causes of death in Europe/N. AmericaClinical course characterised by infective exacerbations (Haemophilus

influenzae

, Streptococcus pneumoniae)Death by respiratory failure or heart failure (“

cor pulmonale”)Slide73

Chronic Bronchitis

Cough productive of sputum on most days for 3 months of at least 2 successive yearsAn epidemiological definitionDoes not imply airway inflammationSlide74

Chronic Bronchitis

Chronic irritation defensive increase in mucus production with increase in numbers of epithelial cells (esp goblet cells)Poor relation to functional obstructionRole in sputum production and increased tendency to infectionSlide75

Chronic

BronchitisNon-reversible obstructionIn some patients there may be a reversible (“asthmatic”) componentSlide76

Normal vs. Chronic BronchitisSlide77

Small airways in Chronic Bronchitis

More important than traditionally realizedGoblet cell

metaplasia

, macrophage accumulation and

fibrosis around bronchioles may generate functional obstructionSlide78

Emphysema

Increase beyond the normal in the size of the airspaces distal to the terminal bronchioleWithout fibrosisThe gas-exchanging compartment of the lungSlide79

Emphysema (types)

Centriacinar (centrilobular)PanacinarOthers (e.g. localized around scars in the lung)Slide80

Centriacinar

(centrilobular)

Begins in the respiratory bronchioles and spreads peripherally.

Associated with long-standing cigarette smoking and predominantly involves the upper half of the lungsSlide81

Panacinar

Emphysema Destroys the entire alveolus uniformly and is predominant in the lower half of the lungs. Generally is observed in patients with homozygous

a

1 antitrypsin (AAT) deficiency.

In people who smoke focal

panacinar emphysema at the lung bases may accompany centriacinar

emphysema.Slide82

Normal lungSlide83

There are two major types of emphysema:

centrilobular

(

centriacinar

) and panlobular

(panacinar). Slide84

Centrilobular

emphysema "dirty holes” This pattern is typical for smokers. Slide85

Remaining Airspaces are Dilated.Slide86

Centriacinar

emphysemaSlide87

Panacinar

emphysema 2Slide88

Panacinar

emphysema 1Slide89

Emphysema

Difficult to diagnose in life (apart from late disease – enlarged “barrel chest”)Radiology (CT) can show changes in lung densityCorrelation with function known from autopsy studiesSlide90

Emphysema

“Dilatation” is due to loss of alveolar walls (tissue destruction)Appears as “holes” in the lung tissueSlide91

Emphysema

How do these changes relate to functional deficit?Poorly at macroscopic levelBetter with microscopic measurementSlide92

NormalSlide93

Early emphysemaSlide94

Emphysema Impairs Respiratory Function

Diminished alveolar surface area for gas exchange (decreased Tco)Loss of elastic recoil and support of small airways leading to tendency to collapse with obstructionSlide95

Loss of surface area (emphysema)Slide96

As disease advances….

PaO2 leads to:

Dyspnea

and increased respiratory rate

Pulmonary vasoconstriction (and pulmonary hypertension)Slide97
Slide98

Epidemiology of COPD

SmokingAtmospheric pollutionGenetic factorsSlide99

Pathophysiology

of EmphysemaHigh rate of emphysema in the rare genetic condition of

a

1 antitrypsin deficiency

THE PROTEASE/ANTIPROTEASE HYPOTHESIS Slide100

Elastic Tissue

Sensitive to damage by elastases (enzymes produced by neutrophils and macrophages)

a

1 antitrypsin

acts as an anti-elastase

Imbalance in either arm of this system predisposes to destruction of elastic alveolar walls (emphysema)Slide101

Tobacco smoke…..

Increases #’s of neutrophils

and macrophages in lung

Slows transit of these cells

Promotes neutrophil

degranulationInhibits

a

1 antitrypsinSlide102

Classification and Spread of Fungi

Yeasts

Are round and grow by budding

Molds

Form tubular structures called

hyphae

Grow by branching and forming spores

Dimorphic fungi

Grow as yeasts at body temperatures and as molds at room temperatures

Mechanisms of fungal spread

Inhalation of sporesSlide103

Farmer’s LungSlide104

Silo Filler’s DiseaseSlide105

Laboratory Tests to Diagnose

Histoplasmosis

Cultures

Fungal stain

Antigen detection

Serologic tests for antibodiesSlide106

AsbestosSlide107

The dense white encircling tumor mass is arising from the visceral pleura and is a

mesothelioma

. Slide108

Respiratory Disorders in the Neonate

Respiratory distress syndromeBronchopulmonary dysplasiaSlide109

Respiratory Disorders in Children

Upper airway infectionsViral croupSpasmodic croupEpiglottisLower airway infectionsAcute bronchiolitisSlide110

Impending Respiratory Failure in Infants and Children

Rapid breathingExaggerated use of the accessory muscles

Retractions

Nasal flaring

Grunting during expiration Slide111

Question

The lungs are a common site of secondary tumor development. Why?Due to the highly vascular nature and small capillaries

Due to the fragility of the cells

Due to the rapid replication of type I alveolar cells

Due to dumb luckSlide112

Answer

Due to the highly vascular nature and small capillaries

Due to the fragility of the cells

Due to the rapid replication of type I alveolar cells

Due to dumb luckSlide113

Disorders of Ventilation and

Gas ExchangeSlide114

Gases of Respiration

Primary function of respiratory systemRemove CO

2

Add of O

2

Insufficient exchange of gases

Hypoxemia

HypercapniaSlide115

Hypoxemia

Hypoxemia results from

Inadequate O

2

in the air

Diseases of the respiratory system

Dysfunction of the neurological system

Alterations in circulatory function

Mechanisms

Hypoventilation

Impaired diffusion of gases

Inadequate circulation of blood through the pulmonary capillaries

Mismatching of ventilation and perfusion

Slide116

Manifestations of Hypoxemia

Mild hypoxemiaMetabolic acidosis

Increase in heart rate

Peripheral vasoconstriction

Diaphoresis

Increase in blood pressure

Slight impairment of mental performanceSlide117

Manifestations of Hypoxemia (cont.)

Chronic hypoxemia

Manifestations of chronic hypoxia may be insidious

in onset and attributed to other causes

Compensation masks condition

Increased ventilation

Pulmonary vasoconstriction

Increased production of red blood cells

CyanosisSlide118

Hypercapnia

Increased arterial PCO

2

Caused by

hypoventilation or mismatching of ventilation and perfusion

Effects

Acid-base balance (decreased pH, respiratory acidosis)

Kidney function

Nervous system function

Cardiovascular function

Slide119

Causes of Disorders of Lung Inflation

Conditions that produce lung compression or lung collapseCompression of the lung by an accumulation of fluid in the intrapleural space

Complete collapse of an entire lung as in

pneumothorax

Collapse of a segment of the lung as in

atelectasisSlide120

Characteristics and Symptoms

of Pleural PainAbrupt in onsetUnilateral, localized to lower and lateral part of the chestMay be referred to the shoulder

Usually made worse by chest movements

Tidal volumes are kept small.

Breathing becomes more rapid.Reflex splinting of the chest may occur.Slide121

Pleural Effusion

DefinitionAn abnormal collection of fluid in the pleural cavity

Types of fluid

Transudate

Exudate

Purulent drainage (empyema)

Chyle

BloodSlide122

Diagnosis and Treatment

of Pleural EffusionDiagnosis

Chest radiographs, chest ultrasound

Computed tomography (CT)

Treatment:

directed at the cause of the disorder

Thoracentesis

Injection of a sclerosing agent into the pleural cavity

Open surgical drainageSlide123

Disorders of the Pleura

Pleural effusion: abnormal collection of fluid in the pleural cavity

Transudate or exudate, purulent (containing pus), chyle, or sanguineous (bloody)

HemothoraxPleuritis

Chylothorax

Atelectasis

EmpyemaSlide124

Types of Pneumothorax

Spontaneous pneumothorax Occurs when an air-filled blister on the lung surface rupturesTraumatic pneumothoraxCaused by penetrating or nonpenetrating injuries

Tension pneumothorax

Occurs when the intrapleural pressure exceeds atmospheric pressureSlide125

Atelectasis

Definition

Incomplete expansion of a lung or portion of a lung

Causes

Airway obstruction

Lung compression such as occurs in

pneumothorax

or pleural effusion

Increased recoil of the lung due to loss of pulmonary surfactantSlide126

Types of

Atelectasis

Primary

Present at birth

Secondary

Develops in the neonatal period or later in life Slide127

Question

Which of the following is a disorder caused by abnormal accumulation of fluid in the pleural space?Pneumothorax

Pleural effusion

Atelectasis

Hypercapnia Slide128

Answer

PneumothoraxPleural diffusion: Pleural diffusion can be caused by

transudate

,

exudate, chyle

, or other fluid. Atelectasis

Hypercapnia

Slide129

Physiology of Airway Disease

Upper respiratory tractTrachea and major bronchi

Lower respiratory tract

Bronchi and alveoli

Creation of negative pressureEffects of CO

2/pH

Role of inflammatory mediators

Increase airway responsiveness by

Producing bronchospasm

Increasing mucus secretion

Producing injury to the mucosal lining of the airwaysSlide130

Functions of Bronchial Smooth Muscle

The tone of the bronchial smooth muscles surrounding the airways determines airway radius.The presence or absence of airway secretions influence airway patency.

Bronchial smooth muscle is innervated by the autonomic nervous system.

Parasympathetic: vagal control

Bronchoconstrictor

Sympathetic: 

2

-adrenergic receptors

BronchodilatorSlide131

Factors Involved in the

Pathophysiology of AsthmaGenetic

Atopy

Early vs. late phase

Environmental

Viruses

Allergens

Occupational exposureSlide132

Factors Contributing to the Development of an Asthmatic Attack

AllergensRespiratory tract infections

Exercise

Drugs and chemicals

Hormonal changes and emotional upsets

Airborne pollutants

Gastroesophageal

refluxSlide133

Classifications of Asthma Severity

Mild intermittentMild persistentModerate persistentSevere persistentSlide134

Question

Which of the following have not been implicated in the development of asthma?

Allergens

Respiratory tract infections

Diet

Drugs and chemicals

Hormonal changes and emotional upsets

Airborne pollutants

Gastroesophageal

refluxSlide135

Answer

Allergens

Respiratory tract infections

Diet: Diet does not affect the respiratory tract other than via allergic reactions.

Drugs and chemicals

Hormonal changes and emotional upsets

Airborne pollutants

Gastroesophageal

refluxSlide136

Chronic Obstructive Airway Disease

Inflammation and fibrosis of the bronchial wall

Hypertrophy of the

submucosal

glands

Hypersecretion

of mucus

Loss of elastic lung fibers

Impairs the expiratory flow rate, increases air trapping, and predisposes to airway collapse

Alveolar tissue

Decreases the surface area for gas exchange

Slide137

Causes of Chronic Obstructive Airway Disease

Chronic bronchitisEmphysema

Bronchiectasis

Cystic fibrosisSlide138

Bronchiectasis

occurs when there is obstruction or infection with inflammation and destruction of bronchi so that there is permanentSlide139
Slide140

Pulmonary Fibrosis

The

alveolitis

that produces fibroblast proliferation and collagen deposition is progressive over time.

SarcoidosisSlide141

Honeycomb LungSlide142

Characteristics of Type A Pulmonary Emphysema

Smoking historyAge of onset: 40–50 yearsOften dramatic barrel chest

Weight loss

Decreased breath sounds

Normal blood gases until late in disease process

Cor

pulmonale

only in advanced cases

Slowly debilitating diseaseSlide143
Slide144

Characteristics of Type B Chronic Bronchitis

Smoking historyAge of onset 30–40 yearsBarrel chest may be presentShortness of breath predominant early symptomRhonchi

often present

Sputum frequent early manifestationSlide145

Characteristics of Type B Chronic Bronchitis (cont.)

Often dramatic cyanosisHypercapnia and hypoxemia may be presentFrequent cor pulmonale

and

polycythemia

Numerous life-threatening episodes due to acute exacerbationsSlide146

Types of Chronic Obstructive Pulmonary Disease

EmphysemaEnlargement of air spaces and destruction of lung tissue

Types:

centriacinar

and

panacinar

Chronic obstructive bronchitis

Obstruction of small airways Slide147

Bronchiectasis

Permanent dilation of the bronchi and bronchioles

Secondary to persisting infection or obstruction

Manifestations

Atelectasis

Obstruction of the smaller airways

Diffuse bronchitis

Recurrent

bronchopulmonary

infection

Coughing; production of copious amounts of foul-smelling, purulent sputum;

hemoptysis

Weight loss and anemia are common.Slide148

Cystic Fibrosis

Definition

An

autosomal

-recessive disorder involving fluid secretion in the exocrine glands and the epithelial lining of the respiratory, gastrointestinal, and reproductive tracts

Cause

Mutations in a single gene on the long arm of chromosome 7 that encodes for the cystic fibrosis

transmembrane

regulator (CFTR), which functions as a chloride (

Cl

-

) channel in epithelial cellsSlide149

Manifestations of Cystic Fibrosis

Pancreatic exocrine deficiencyPancreatitis

Elevation of sodium chloride in the sweat

Excessive loss of sodium in the sweat

Nasal polyps

Sinus infections

Cholelithiasis

Slide150

Diffuse Interstitial Lung Diseases

Definition

A diverse group of lung disorders that produce similar inflammatory and fibrotic changes in the

interstitium

or

interalveolar

septa of the lung

Types

Sarcoidosis

Occupational lung diseases

Hypersensitivity

pneumonitis

Lung diseases caused by exposure to toxic drugs Slide151

Occupational Lung Diseases

Pneumoconioses

Caused by inhalation of inorganic dusts and particulate matter

Hypersensitivity diseases

Caused by inhalation of organic dusts and related occupational antigens

Byssinosis

: occurs in cotton workers; has characteristics of the

pneumoconioses

and hypersensitivity lung diseaseSlide152

Pulmonary Embolism

Development

A blood-borne substance lodges in a branch of the pulmonary artery and obstructs the flow

Types

Thrombus:

arising from deep vein thrombosis

Fat:

mobilized from the bone marrow after a fracture or from a traumatized fat depot

Amniotic fluid:

enters the maternal circulation after rupture of the membranes at the time of deliverySlide153

Pulmonary EmbolismSlide154

Saddle EmbolusSlide155
Slide156
Slide157

Pulmonary Hypertension

Signs and symptoms of secondary pulmonary hypertension

Dyspnea

and fatigue

Peripheral edema

Ascites

Signs of right heart failure (

cor

pulmonale

)

A disorder characterized by an elevation of pressure within the pulmonary circulation

Pulmonary arterial hypertensionSlide158

Causes of Acute Respiratory Distress Syndrome

Aspiration of gastric contents

Major trauma (with or without fat emboli)

Sepsis secondary to pulmonary or

non-pulmonary

infections

Acute pancreatitis

Hematologic disorders

Metabolic events

Reactions to drugs and toxinsSlide159
Slide160

Causes of Respiratory Failure

Impaired ventilationUpper airway obstruction

Weakness of paralysis of respiratory muscles

Chest wall injury

Impaired matching of ventilation and perfusion

Impaired diffusion

Pulmonary edema

Respiratory distress syndromeSlide161

Treatment of Respiratory Failure

Respiratory supportive care directed toward maintenance of adequate gas exchange

Establishment of an airway

Use of

bronchodilating

drugs

Antibiotics for respiratory infections

Ensure adequate oxygenationSlide162

Question

Which of the following has been implicated as a causative factor in right ventricular failure?Cor

pulmonale

Pneumothorax

Cystic

fibrosis

Acute respiratory distress syndromeSlide163

Answer

Cor

pulmonale

:

Cor

pulmonale

will result in right ventricle failure due to the increase in workload.

Pneumothorax

Cystic fibrosis

Acute respiratory distress syndromeSlide164

Question

The most common port of entry for cold viruses is _______.InhalationSmall cuts

Food

Conjunctival surface of the eyes

FingersSlide165

Answer

The most common port of entry for cold viruses is _______.

Inhalation

Small cuts

Food

Conjunctival

surface of the eyes

FingersSlide166

Factors Affecting the Signs and Symptoms of Respiratory Tract Infections

The function of the structure involvedThe severity of the infectious process

The person’s age and general health statusSlide167

Rhinitis and Sinusitis

Rhinitis Inflammation of the nasal mucosa

Sinusitis

Inflammation of the

paranasal

sinusesSlide168

Types of Sinuses

Paranasal sinuses

Air cells connected by narrow openings or

ostia

with the superior, middle, and inferior nasal

turbinates

of the nasal cavity

Maxillary sinus

Inferior to the bony orbit and superior to the hard palate

Its opening is located superiorly and medially in the sinus, a location that impedes drainage.

Frontal sinuses

Open into the middle

meatus

of the nasal cavitySlide169

Transmission

of Common ColdViral infection of the upper respiratory tract

Rhinoviruses,

parainfluenza

viruses, respiratory

syncytial

virus,

coronaviruses

, and adenoviruses

Fingers are the greatest source of spread

Coughing, sneezing

The nasal mucosa and

conjunctival

surface of the eyes are the most common portals of entry for the virus.

Slide170

Types of Sinuses (cont.)

Sphenoid sinus

Just anterior to the pituitary

fossa

behind the posterior

ethmoid sinuses

Its paired openings drain into the

sphenoethmoidal

recess at the top of the nasal cavity.

Ethmoid

sinuses

Comprise 3–15 air cells on each side, with each maintaining a separate path to the nasal chamberSlide171

Allergic

RhinosinusitisOccurrence

Occurs in conjunction with allergic rhinitis

Mucosal changes are the same as allergic rhinitis

Symptoms

Nasal stuffiness, itching and burning of the nose, frequent bouts of sneezing, recurrent frontal headache, watery nasal discharge

Treatment

Oral antihistamines, nasal decongestants, and intranasal

cromolynSlide172

Answer

Inhalation

Small cuts

Food

Conjunctival surface of the eyes: The eyes and the nasal mucosa are the most common ports of entry.

FingersSlide173

Types of Influenza Viruses

Type AMost common type

Can infect multiple species

Causes the most severe disease

Further divided into subtypes based on two surface antigens: hemagglutinin (H) and neuraminidase (N)

Type B

Has not been categorized into subtypesSlide174

Lung Cancer

Causative factorsSmokingAsbestos

Familial predisposition

Primary lung tumors (95%) vs. bronchial, glandular, lymphoma

Secondary via metastasisSlide175

Categories of

Bronchogenic Carcinomas

Squamous

cell lung carcinoma (25–40%)

Closely related to smoking

Adenocarcinoma

(20–40%)

Most common in North America

Small cell carcinoma (20–25%)

Small round to oval cells, highly malignant

Large cell carcinoma (10–15%)

Large polygonal cells, spread early in developmentSlide176

Squamous

Cell CarcinomaSlide177
Slide178
Slide179

This is another

sqamous

cell carcinoma that extends from

hilum

to pleura. The black areas represent anthracotic

pigment trapped in the tumor.Slide180

AdenocarcinomaSlide181

Bronchioalveolar

CarcinomaSlide182

Categories of the Manifestation of Lung Cancer

Those due to involvement of the lung and adjacent structures

The effects of local spread and metastasis

The

nonmetastatic

paraneoplastic

manifestations involving endocrine, neurologic, and connective tissue function

Nonspecific symptoms such as anorexia and weight lossSlide183

Metastatic Lung CancerSlide184
Slide185

Classifications of

RhinosinusitisAcute rhinosinusitis

May be of viral, bacterial, or mixed viral-bacterial origin

May last from 5 to 7 days up to 4 weeks

Subacute rhinosinusitis

Lasts from 4 weeks to less than 12 weeks

Chronic rhinosinusitis

Lasts beyond 12 weeksSlide186
Slide187

Control of Breathing

Respiratory centerPacemaker centerPneumotaxic centerApneustic centerPhrenic nerveSlide188

Control of Breathing (cont.)

Automatic regulation of ventilation Controlled by input from two types of sensors or receptors

Chemoreceptors:

monitor blood levels of oxygen and carbon dioxide and adjust ventilation to meet the changing metabolic needs of the body

Lung receptors:

monitor breathing patterns and lung functionSlide189

Control of Breathing (cont.)

Voluntary regulation of ventilation

Integrates breathing with voluntary acts such as speaking, blowing, and singing

These acts, initiated by the motor and premotor cortex, cause a temporary suspension of automatic breathing.Slide190

Cough Reflex

Neurally mediated reflex that protects the lungs Accumulation of secretions

Entry of irritating and destructive substances

Slide191

Cheyne

-Stokes Abnormal pattern of breathing Characterized by oscillation of ventilation between apnea and hyperpnea

Compensate for changing serum partial pressuresSlide192

Mechanisms Involved in

Dyspnea

Stimulation of lung receptors

Increased sensitivity to changes in ventilation perceived through central nervous system mechanisms

Reduced

ventilatory

capacity or breathing reserve

Stimulation of neural receptors in the muscle fibers of the intercostals and diaphragm and of receptors in the skeletal joints

Associated conditions

Primary lung diseases

Heart disease

Neuromuscular disorders

Slide193

Question

Which of the following accurately describes your breathing pattern after running to class?Cheyne-Stokes

Normal

Dyspnea

Eupnea

HypoxemiaSlide194

Answer

Cheyne-Stokes

Normal

Dyspnea: Dyspnea is simply labored breathing; it is not necessarily pathological in nature.

Eupnea

HypoxemiaSlide195

Stages of Lung Development

Embryonic periodPseudoglandular periodCanicular period

Saccular period

Alveolar periodSlide196

Function of the Respiratory System

Gas exchangeOxygen from air to lungs

Carbon dioxide from blood to atmosphere

Host defense

Barrier to outside environment

Metabolic organ

Synthesizes and metabolizes different componentsSlide197

Structural Organization of the Respiratory System

Consists of the air passages and the lungsDivided into two parts by function:

Conducting airways,

through which air moves as it passes between the atmosphere and the lungs

Respiratory tissues of the lungs,

where gas exchange takes placeSlide198

Structures of the Airways

ConductingNasal passages

Mouth and pharynx

Larynx

Trachea

Bronchi

Bronchioles

Mucociliary blanket

Respiratory tissues

Alveolar bundle

Respiratory membraneSlide199

Ventilation

Depends on the conducting airwaysNasopharynx and oropharynxLarynxTracheobronchial treeFunctionMoves air out of the lungs but does not participate in gas exchangeSlide200

Structure and Function of the Larynx

StructureConnects the oropharynx with the trachea

Located in a strategic position between the upper airways and the lungs

Functions

Helps produce speech

Protects the lungs from substances other than airSlide201

Structures of the Lungs

Soft, spongy, cone-shaped organs located side by side in the chest cavitySeparated from each other by the mediastinum and its contents

Divided into lobes (3 in the right lung, 2 in the left)

Apex:

upper part of the lung; lies against the top of the thoracic cavity

Base:

lower part of the lung; lies against the diaphragmSlide202

Composition of the Alveolar Structures

Type I alveolar cells Flat, squamous epithelial cells across which gas exchange takes place

Type II alveolar cells

Produce surfactant, a lipoprotein substance that decreases the surface tension in the alveoli and allows for greater ease of lung inflationSlide203

Normal LungSlide204

Lung Circulation

Pulmonary circulation

Arises from the pulmonary artery

Provides for the gas exchange function of the lungs

Bronchial circulation

Arises from the thoracic aorta

Supplies the lungs and other lung structures with oxygen

Distributes blood to the conducting airways

Warms and humidifies incoming air Slide205

Ventilation and Gas Exchange

VentilationThe movement of gases into and out of the lungsInspirationAir is drawn into the lungs as the respiratory muscles expand the chest cavity.Expiration

Air moves out of the lungs as the chest muscles recoil and the chest cavity becomes smaller.Slide206

Question

Which of the following is directly responsible for gas exchange?Trachea

Bronchi

Bronchial circulation

Pulmonary circulation

Respiratory membraneSlide207

Answer

Trachea

Bronchi

Bronchial circulation

Pulmonary circulation

Respiratory membrane: The respiratory membrane is the anatomical site of gas exchange in the lungs. It is located in the alveoli.Slide208

Properties of Gases

Respiratory pressures Atmospheric pressurePartial pressuresHumidity

Temperature effectsSlide209

Respiratory Pressures

Intrapulmonary pressure or alveolar pressurePressure inside the airways and alveoli of the lungs

Intrapleural pressure

Pressure in the pleural cavity

Intrathoracic pressure

Pressure in the thoracic cavitySlide210

Lung Compliance

Lung compliance C = ΔV/ΔP

The change in lung volume (ΔV) that can be accomplished with a given change in respiratory pressure (ΔP)Slide211

Airway Resistance

The volume of air that moves into and out of the air-exchange portion of the lungs

Directly related to the pressure difference between the lungs and the atmosphere

Inversely related to the resistance the air encounters as it moves through the airwaysSlide212

Lung function tests

Tidal volume (TV):

it is the amount of gas inhaled or exhaled with each resting breath.

Residual volume (RV):

it is the amount of gas remaining in the lungs at the end of maximum exhalation.Slide213

Vital capacity (VC):

it is the total amount of gas that can exhaled following maximum inhalation.

Total lung capacity (TLC):

it is the amount of gas in the lung at the end of maximum inhalation.

TLC = RV+ VCSlide214

Pulmonary Function Studies

Maximum voluntary ventilation The volume of air a person can move into and out of the lungs during maximum effort lasting for 12–15 seconds

Forced expiratory vital capacity (FVC)

Involves full inspiration to total lung capacity followed by forceful maximal expirationSlide215

Pulmonary Function Studies (cont.)

Forced expiratory volume (FEV) The expiratory volume achieved in a given time period

Forced

inspiratory

vital flow (FIF)

The respiratory response during rapid maximal inspiration Slide216

Processes of Pulmonary Gas Exchange

Ventilation The flow of gases into and out of the alveoli of the lungs

Perfusion

The flow of blood in the adjacent pulmonary capillaries

Diffusion

Transfer of gases between the alveoli and the pulmonary capillariesSlide217

Types of Dead Space

Anatomic dead spaceThat contained in the conducting airways

Alveolar dead space

That contained in the respiratory portion of the lung

Physiologic dead space

The anatomic dead space plus the alveolar dead space Slide218

Matching Ventilation and Perfusion

Required for exchange of gases between the air in the alveoli and the blood in pulmonary capillaries Two factors interfere with the process:Dead air space and shuntThe blood oxygen level reflects the mixing of blood from alveolar dead space and physiologic shunting areas as it moves into the pulmonary veins.Slide219

Factors Affecting Alveolar–Capillary Gas Exchange

Surface area available for diffusionThickness of the alveolar-capacity membranePartial pressure of alveolar gasesSolubility and molecular weight of the gasSlide220

Oxygen and Carbon Dioxide Transport

PO

2

of arterial blood normally is above 80 mm Hg.

In chemical combination with hemoglobin

98–99%

Oxyhemoglobin

Binding affinity of hemoglobin for oxygen

In the dissolved state Slide221

Oxygen and Carbon Dioxide Transport

(cont.)The PCO

2

is in the range of 35–45 mm Hg.

Dissolved in carbon dioxide (10%)

Attached to hemoglobin (30%)

Bicarbonate (60%)

Acid-base balance is influenced by the amount of dissolved carbon dioxide and the bicarbonate level in the bloodSlide222
Slide223

Dead Space

Area where gas exchange cannot occurIncludes most of airway volumeAnatomical dead space (=150 ml)

Airways

Physiological dead space

= anatomical + non functional alveoli

Calculated using a pure O2 inspiration and measuring nitrogen in expired air (fig 37-7)% area X VeSlide224

Alveolar Volume

Alveolar volume (2150 ml) = FRC (2300 ml)- dead space (150 ml)At the end of a normal expiration most of the FRC is at the level of the alveoliSlow turnover of alveolar air (6-7 breaths)Rate of alveolar ventilation

Va

= RR (

Vt-Vd) Slide225

Types of Shunts

Anatomic shuntBlood moves from the venous to the arterial side of the circulation without moving through the lungs

Physiologic shunt

Mismatching of ventilation and perfusion with the lung

Results in insufficient ventilation to provide the oxygen needed to oxygenate the blood flowing through the alveolar capillariesSlide226

Matching

Ventilation and PerfusionRequired for exchange of gases between the air in the alveoli and the blood in pulmonary capillaries

Two factors interfere with the process:

Dead air space and shunt

The blood oxygen level reflects the mixing of blood from alveolar dead space and physiologic shunting areas as it moves into the pulmonary veins.Slide227

Ventilation

-Perfusion DefectsAlveoli that are ventilated but not

perfused

is

ventilatory “dead space”Alveoli that are

perfused but not ventilated leads to “shunting” of non-oxygenated blood from pulmonary to systemic circulation ( a mechanism of cyanosis)Slide228

ANS influence on pulmonary vascular smooth muscle

SNS + will cause a mild vasoconstriction3 Hz to 30 Hz



pulmonary arterial BP about 30%Mediated by alpha receptors

With alpha blockage response abolished and at 30 Hz. vasodilatation observed as beta receptors are unmaskedParasympathetic + will cause a mild vasodilatation

(major constrictor effect on pulmonary vascular smooth muscle is low alveolar O2)