RESPIRATORY SYSTEM

Stanley C. Luces MD

OBJECTIVES Describe the structures and functions of the upper and lower respiratory tracts

Describe ventilation, perfusion, diffusion, shunting, and relationship of pulmonary circulation to these processes.

Discriminate between normal and abnormal breath sounds

Use assessment parameters appropriate for determining the characteristics and severity of the major symptoms of respiratory dysfunctions.

Identify the implications of the various procedures used for diagnostic evaluation of respiratory function.

THE RESPIRATORY SYSTEM

The Respiratory SystemMajor function is RESPIRATIONa. Gas exchangeb. Regulation of blood pHc. Voice productiond. Olfactione. Innate immunityCommonly divided into

UPPER RESPIRATORY tract and LOWER RESPIRATORY tract

Respiratory Anatomy

Respiratory Anatomy

Respiratory Anatomy

The UPPER Respiratory tract

The nose, pharynx and larynx

The LOWER respiratory tract

Composed of the trachea down to the Lungs

The Respiratory System air conducting unit respiratory

unit

The NOSEThe NASAL cavity is made up of bones, cartilages and turbinates or conchaeThe nostril is the external openingThe choanae is the internal opening

Functions of the nose1. Hairs or vibrissae filter large particles2. Blood vessels warm the air3. Mucus serves to humidify the air4. Phonation

The Paranasal sinusesAir-filled spaces in the skullServes as resonators

The PharynxMusculo-membranous tube from behind the nasal cavity to the level of the cricoid cartilage (C6)

The Pharynx3 component parts

1. Nasopharynx2. Oropharynx3. Laryngopharynx

The pharynxThe pharynx functions

1. As passageway for both air and foods (in the oropharynx)2. To protect the lower airway

The LarynxUpper expanded portion of the tracheaMade up of cartilagesFunction: air passageway and phonation

The vocal cords1. False vocal cords2. True vocal cords3. Glottis- the space between the true vocal cords and is the narrowest portion of the adult airway

Lower Respiratory Tract

Lower airway: TracheaCalled windpipeMade up of 15-20 C-shaped cartilageLined with pseudostratified ciliated columnar epitheium

BronchusRIGHT Bronchus

WideShortSlightly vertical

LEFT BronchusNarrowLongSlightly horizontal

BronchiolesPrimary bronchussecondary bronchustertiary bronchus terminal bronchioles

Terminal bronchioles belong to the respiratory unit

Respiratory unitRespiratory bronchiolesAlveolar ductsAlveolar sacsAlveolus

The respiratory AcinusThe respiratory membrane is composed

of two epithelial cells1.The type 1 pneumocyte- most abundant, thin and flat. This is where gas exchange occurs2. The type 2 pneumocyte- secretes the lung surfactantSurfactant:

Surface active agentDetergent that greatly decreases the surface tension of fluid lining the alveoli.

Blood Supply of the lungs

Bronchi & their branches are supplied by the bronchial arteries (branches of aorta)Bronchial Veins: drain into the azygos & hemiazygos vein

The PleuraSurrounds the lungs and provide protection1. Parietal pleura- in the chest wall2. Visceral pleura- intimately attached to the lungs3. Pleural space- in between the two pleurae

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CLINICAL Correlation:Pleural Effusion

___________- Serous fluid in the pleural cavity___________- Blood in the cavity___________- Pus in the cavity___________- Lymph in the cavity

CLINICAL Correlation:Pleural Effusion

Hydrothorax- Serous fluid in the pleural cavity___________- Blood in the cavity___________- Pus in the cavity___________- Lymph in the cavity

CLINICAL Correlation:Pleural Effusion

Hydrothorax- Serous fluid in the pleural cavityHemothorax- Blood in the cavity___________- Pus in the cavity___________- Lymph in the cavity

CLINICAL Correlation:Pleural Effusion

Hydrothorax- Serous fluid in the pleural cavityHemothorax- Blood in the cavityPyothorax/Empyema- Pus in the cavity________- Lymph in the cavity

CLINICAL Correlation:Pleural Effusion

Hydrothorax- Serous fluid in the pleural cavityHemothorax- Blood in the cavityPyothorax- Pus in the cavityChylothorax- Lymph in the cavity

CLINICAL Correlation:Pneumothorax

Accumulation of air in the pleural space

The RIB CAGE

MECHANICS OF BREATHING

A. Muscles of Inspiration1. Diaphragm

- when contracts, abdominal contents are pushed downwards and the ribs are lifted upward & inward

- increasing the volume of thoracic cavity

2. External intercostals- Elevates the ribs and sternum- Increases the thoracic volume

by increasing the diameter of thoracic volume

3. Accessory musclesa. Sternocleidomastoid muscles

b. Scalene c. Pectoralis minor

Muscles of Expiration1. Abdominal muscles- Compress the abdominal cavity

push the diaphragm up, and push air out of the lungs.

2. Internal Intercostal muscles- Pulls the ribs downward and

inward

Respiratory Muscle: diaphragm

Supplied by the phrenic nerveDuring INSPIRATION, it contracts downwardsDuring EXPIRATION, it relaxes and moves upwards

Respiratory Muscles

Respiratory Physiology1. Ventilation and gas exchange2. Mechanics of breathing3. Gas transport4. Pulmonary volumes and capacities5. Respiratory control

Gas exchangeOXYGEN moves by the mechanism of

DIFFUSIONExchange of gases across the respiratory

membranes is influenced by:1. Thickness of the membrane

e.g. pulmonary edema thickness doubled > decreased rate of

diffusion2. Total surface area

e.g. emphysema and lung Ca > restricted gas exchange

3. Concentration gradient for gases across the membrane.

Mechanics of Breathing

"Work" of Breathing

Compliance work - that required to expand the lungs against its elastic forces

Recoil- that required to collapse the lungs

Pulmonary PressuresMajor factors in determining the extent of lung expansion and compliance during the processes of inspiration and expiration:

Alveolar pressureIntrapleural pressureAlveolar surfactant

During inspiration, the thoracic cage enlarges, enlarging both lungs and decreasing the pressures.

Pulmonary PressuresBoyle’s Law:During inspiration, the enlargement of the thoracic cage decreases the pressure in the alveoli to about –3 mmHg. This negative pressure pulls air through the respiratory passageways into the alveoli.

Pulmonary PressuresBoyle’s Law:During expiration, the exact mechanism and effects occur. Compression of the thoracic cage around the lungs increases the alveolar pressure to approximately +3 mmHg which pushes the air out of the alveoli into the atmosphere.

Pulmonary PressuresIntrapleural Pressures:

Intrapleural space is the space between the lungs and the outer walls of the thoracic cavity. The pressure here is ALWAYS a few mmHg less than in the alveoli for the following reasons:

Surface tension of the fluid inside the alveoli always makes the alveoli try to collapse.Elastic fibers spread in all directions through the lung tissues and tend to contract the lungs.

These factors pull the lungs away from the outer walls of the pleural cavity, creating an average negative pressure of –5 mmHg.

Pulmonary PressuresSurfactant:

Surface active agentDetergent that greatly decreases the surface tension of fluid lining the alveoli.

VentilationVentilation is the movement of air into the lungs

Fig. 15.11a

Fig. 15.11b

Control of Respiration: Central

Respiratory center in the medullaControls the rate and depth of respirationIncreased CO2 is the most potent stimulus

Fig. 15.15

Control of Respiration:Peripheral

1. Chemoreceptors in the carotid and aortic bodies

Sensitive to changes in pH and O2Decreased O2 (HYPOXIA) increase respirationDecreased pH (acidosis) increase respiration

2. Hering-Breurer reflexStretch receptors in the lungs limit the inspiration

Fig. 15.16

The Cough and Sneeze Reflexes

The Cough and Sneeze Reflexes

Means for keeping the respiratory passages clean by forcing air very rapidly outward using these two reflexes.Mediated by respiratory muscles, voluntary and involuntary, with regulation by the central nervous system and sensory receptors lining the respiratory tract.

The Cough ReflexIrritant touches the surface of the glottis, trachea or bronchus.

Sensory signals are transmitted to the medulla.

Motor signals are transmitted back to the respiratory system.

The Cough Reflex

Vocal cords open suddenly, allowing pressurized air in thelungs to flow out in a blast.

Respiratory muscles contract rapidly generatinghigh pressures in the lungs while the vocal cords

remain tightly closed.

Motor signals are transmitted back to the respiratory system.

The Sneeze ReflexIrritant comes into contact with sensory receptors in the nose.

Sensory signals are received in the medulla.

Motor signals are generated and transmitted back.

The Sneeze Reflex

Vocal cords open suddenly, allowing pressurized air in thelungs to flow out in a blast through the nose and mouth.

Respiratory muscles contract rapidly generatinghigh pressures in the lungs while the vocal cords

remain tightly closed.

Motor signals are generated and transmitted back.

Cough and sputum production

Cough is a protective reflexSputum production has many stimuliThick, yellow, green or rust-colored bacterial pneumoniaProfuse, Pink, frothy pulmonary edemaScant, pink-tinged, mucoid Lung tumor

CoughFind out whether cough is productive or nonproductive. Note how and when cough began (sudden or gradual).Identify what makes cough better and what makes it worseDetermine how long it has been present and has there been any change in its characteristics

SputumThe goblet cells and mucous glands secrete mucus that coats the interior lung surface. Sputum is composed of mucus, cellular debris, microorganisms, blood, pus, and foreign particles – “is the substance ejected from the lungs by coughing or clearing the throat.”

Sputum Descriptors:

Amount:ScantCopious

Consistency:ThickViscousFrothyMucoidWateryMucopurulentCast

Symptoms of Pulmonary Disease

Persistent coughAlways abnormalChronic persistent cough may be caused by cigarette smoking, asthma, bronchiectasis or COPD.May also be caused by drugs, cardiac disease, occupational agents and psychogenic factors.Complications include (1) worsening of bronchospasm, (2) vomiting, (3) rib fractures, (4) urinary incontinence, and (5) syncope.

Cough and sputum production

Intervention1. Provide adequate hydration2. Administer aerosolized solutions3. advise smoking cessation4. oral hygiene

Wheezing Sound produced when air passes through partially obstructed or narrowed airways on expiration.Determine when wheezing occurs.Find out what makes the client wheeze.Determine whether wheeze is loud enough for others to hear.Ask what helps stop breathing

CyanosisBluish discoloration of the skinA LATE indicator of hypoxiaAppears when the unoxygenated hemoglobin is more than 5 grams/dLCentral cyanosis observe color on the undersurface of tongue and lipsPeripheral cyanosis observe the nail beds, earlobes

CyanosisInterventions:

Check for airway patencyOxygen therapyPositioningSuctioningChest physiotherapyMeasures to increased hemoglobin

HemoptysisExpectoration of blood from the respiratory tractHemoptysis

Often the first indication of serious bronchopulmonary disease.Massive hemoptysis: coughing up of more than 600 ml of blood in 24 hours.

Common causes: Pulmo infection, Lung CA, Bronchiectasis, Pulmo emboliBleeding from stomach acidic pH, coffee ground material

HemoptysisCoughing up of blood or blood tinged sputum. The source of bleeding might be from anywhere in the upper or lower airways or from the lung parenchyma.

Comparing Hemoptysis and Hematemesis

HemoptysisUsually frothyAlkaline pH

HematemesisNever frothyAcidic pH

HemoptysisInterventions:

Keep patent airwayDetermine the causeSuction and oxygen therapyAdminister Fibrin stabilizers like aminocaproic acid and tranexamic acid

Chest painThe chest pain of pulmonary origin can derive from the chest wall, parietal pleura, visceral pleura, or the lung parenchymaIdentify whether chest pain is respiratory or cardiac in origin

Origin Characteristics Possible Causes

Chest wall Well-localized constant ache increasing with movement

Trauma, cough, herpes zoster

Pleura Sharp, abrupt onset increasing with inspiration or with sudden ventilatory effort (cough, sneeze), unilateral

Pleural inflammation (pleurisy), pulmonary infarction, pneumothorax, tumors

Lung Parenchyma

Dull, constant ache, poorly localized

Benign pulmonary tumors, carcinoma, pneumothorax

EpistaxisBleeding from the nose caused by rupture of tiny, distended vessels in the mucus membrane A vast network of capillaries, called Kiesselbach’s plexus, line the mucosa of the nasal cavity.Most common site- anterior septum

Causes:1. trauma2. infection3. Hypertension4. blood dyscrasias , nasal tumor, cardio diseases

- Avoid petrolatum gauze

- posterior plugs – for post. Epistaxis (for 5 days)

- arterial ligation: internal maxillary or ethmoid artery ligation.

- avoid strenuous activity, blowing nose, sneezing, stooping, lifting.

EpistaxisInterventions

1. Position patient: Upright, leaning forward, tilted prevents swallowing and aspiration2. Apply direct pressure. Pinch nose against the middle septum x 5-10 minutes3. If unrelieved, administer topical vasoconstrictors, silver nitrate, gel foams4. Assist in electrocautery and nasal packing for posterior bleeding

Acute Respiratory Failure

Sudden and life-threatening deterioration of the gas-exchange function of the lungsOccurs when the lungs no longer meet the body’s metabolic needs

Acute Respiratory Failure

Defined clinically as:1. PaO2 of less than 50 mmHg2. PaCO2 of greater than 50 mmHg3. Arterial pH of less than 7.35

Acute Respiratory Failure

CAUSESCNS depression- head trauma, sedativesCVS diseases- MI, CHFAirway irritants- smoke, fumesEndocrine and metabolic disorders- myxedema, metabolic alkalosisThoracic abnormalities- chest trauma

Acute Respiratory Failure

PATHOPHYSIOLOGYDecreased Respiratory Drive

Brain injury, sedatives, metabolic disorders impair the normal response of the brain to normal respiratory stimulation

Acute Respiratory Failure

PATHOPHYSIOLOGYDysfunction of the chest wall

Dystrophy, MS disorders, peripheral nerve disorders disrupt the impulse transmission from the nerve to the diaphragm abnormal ventilation

Acute Respiratory Failure

PATHOPHYSIOLOGYDysfunction of the Lung

ParenchymaPleural effusion, hemothorax, pneumothorax, obstruction interfere ventilation prevent lung expansion

Acute Respiratory Failure

ASSESSMENT FINDINGSRestlessnessDyspneaCyanosisAltered respirationAltered mentationTachycardiaCardiac arrhythmiasRespiratory arrest

Acute Respiratory Failure

DIAGNOSTIC FINDINGSPulmonary function testABG=pH below 7.35CXR- pulmonary infiltratesECG- arrhythmias

Acute Respiratory Failure

MEDICAL TREATMENTIntubationMechanical ventilationAntibioticsSteroidsBronchodilators

Acute Respiratory Failure

INTERVENTIONS1. Maintain patent airway 2. Administer O2 to maintain Pa02 at more than 50 mmHg3. Suction airways as required4. Monitor serum electrolyte levels5. Administer care of patient on mechanical ventilation

COPDThese are group of disorders associated with recurrent or persistent obstruction of air passage and airflow, usually irreversible.

COPDAsthmaChronic bronchitisEmphysemaBronchiectasis

COPD: risk factorsThe most common cause of COPD is cigarette smoking.Others- fumes, air pollution

COPDThe general pathophysiologyIn COPD there is airflow limitation

that is both progressive and associated with abnormal inflammatory response of the lungs

ASTHMAThe acute episode of airway obstruction is characterized by airway hyperactivity to various stimuli

Asthma Pathophysiology

Immunologic/allergic reaction results in histamine release, which produces three main airway responses

a. Edema of mucous membranesb. Spasm of the smooth muscle of

bronchi and bronchiolesc. Accumulation of tenacious

secretions

Asthma Assessment Findings

Assessment findings: history1. Family history of allergies2. Client history of eczema

Asthma Assessment Findings

Assessment findingsRespiratory distressShortness of breathExpiratory wheezeUse of accessory musclesIrritabilitydiaphoresis, cough, anxiety, weak

pulse

EmphysemaThere is progressive and irreversible alveolar destruction with abnormal alveolar enlargement

Emphysema

The result is INCREASED lung compliance, DECREASED oxygen diffusion and INCREASED airway resistance!

Emphysema

These changes cause a state of carbon dioxide retention, hypoxia, and respiratory acidosis.

Emphysema Cigarette smoking

Heredity, Bronchial asthmaAging process

Disequilibrium between

ELASTASE & ANTIELASTASE (alpha-1-antitrypsin)

Destruction of distal airways and alveoliOverdistention of ALVEOLI

Hyper-inflated and pale lungs

Air trapping, decreased gas exchange and Retention of CO2

Hypoxia Respiratory acidosis

Emphysema Assessment

1. Anorexia, fatigue, weight loss

2. Feeling of breathlessness, cough

3. sputum production, flaring of the nostrils

4. Dyspnea5. Barrel chest

Emphysema Assessment

Hyper-resonance in percussion, decreased breath sounds with prolonged expirationDiagnostic tests: pCO2 elevated, PO2 normal or slightly decreased

Chronic bronchitisChronic inflammation of the bronchial air passageway characterized by the presence of cough and sputum production for at least 3 months in each 2 consecutive years.

Chronic Bronchitis pathophysiology

Characteristic changes include:

Hypertrophy/ hyperplasia of the mucus-secreting glands in the bronchi

Decreased ciliary activity, chronic inflammation

Narrowing of the small airways.

Chronic Bronchitis Assessment

1. Productive (copious) cough, dyspnea on exertion, use of accessory muscles of respiration, scattered rales and rhonchi2. Feeling of epigastric fullness, cyanosis, distended neck veins, edema3. Diagnostic tests: increased pCO2 decreased PO2

Bronchiectasis Permanent abnormal

dilation of the bronchi with destruction of muscular and elastic structure of the bronchial wall

Bronchiectasis Caused by bacterial infection or

recurrent lower respiratory tract infections

congenital defects (altered bronchial structures)

lung tumors

Bronchiectasis: assessment

1. Chronic cough with production of mucopurulent sputum, hemoptysis, exertional dyspnea, wheezing

2. Anorexia, fatigue, weight loss3. Diagnostic tests

Bronchoscopy reveals sources and sites of secretions

COPDCOPD Major

PathophysiologyMajor Manifestation

Asthma Bronchial hypersensitivity

Wheezing (reversible)

Emphysema Distal airway DESTRUCTION

BARREL CHEST and thin body

Bronchitis Hyper-secretion of Mucus and inflammation

Abundant muco-purulent sputum and cough, Cor pulmonale

Bronchiectasis

Chronic destruction of bronchus

Hemoptysis and infection

COPD Management1. Rest- To reduce oxygen

demands of tissues

2. Increase fluid intake- To liquefy mucus secretions

3. Good oral care- To remove sputum and prevent infection

COPD Management4. Diet

High caloric diet provides source of energyHigh protein diet helps maintain integrity of alveolar wallsModerate fatsLow carbohydrate diet limits carbon dioxide production (natural end product).

COPD Management5. O2 therapy 1 to 3 lpm (2

lpm is safest)Do not give high concentration of oxygen. The drive for breathing may be depressed.

COPD Management6. Avoid cigarette smoking,

alcohol, and environmental pollutants.

7. CPT –percussion, vibration, postural drainage

COPD Management8. Bronchial hygiene measures

Steam inhalationAerosol inhalation

COPD ManagementPharmacotherapy1. Expectorants (guaiafenessin)/

mucolytic (mucomyst/mucosolvan)

2. AntitussivesDextrometorphanCodeine

COPD ManagementPharmacotherapy3. Bronchodilators

Aminophylline (Theophylline)Ventolin (Salbutamol)Bricanyl (Terbutaline)Alupent (Metaproterenol)

Observe for tachycardia

Bronchodilators

Types Examples Action

Beta 2 agonists

SalbutamolTerbutaline

Stimulate Beta 2 receptor in bronchus

Direct Bronchodilator

AminophyllineTheophylline

Relaxes bronchial smooth muscle

Anti-cholinergic

Ipratropium Blocks parasympathetic system

COPD ManagementPharmacotherapy4. Antihistamine

Benadryl (Diphenhydramine)Observe for drowsiness

5. SteroidsAnti-inflammatory effect

6. Antimicrobials

Oxygenation

Thank you … have a nice day!!!