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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 System


Major function is RESPIRATION a. Gas exchange b. Regulation of blood pH c. Voice production d. Olfaction e. Innate immunity Commonly 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 NOSE
The NASAL cavity is made up of bones, cartilages and turbinates or conchae The nostril is the external opening The choanae is the internal opening

Functions of the nose


1. Hairs or vibrissae filter large particles 2. Blood vessels warm the air 3. Mucus serves to humidify the air 4. Phonation

The Paranasal sinuses


Air-filled spaces in the skull Serves as resonators

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

The Pharynx
3 component parts 1. Nasopharynx 2. Oropharynx 3. Laryngopharynx

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

The Larynx
Upper expanded portion of the trachea Made up of cartilages Function: air passageway and phonation

The vocal cords


1. False vocal cords 2. True vocal cords 3. Glottis- the space between the true vocal cords and is the narrowest portion of the adult airway

Lower Respiratory Tract

Lower airway: Trachea


Called windpipe Made up of 15-20 C-shaped cartilage Lined with pseudostratified ciliated columnar epitheium

Bronchus
RIGHT Bronchus Wide Short Slightly vertical LEFT Bronchus
Narrow Long Slightly horizontal

Bronchioles
Primary bronchussecondary bronchustertiary bronchus terminal bronchioles
Terminal bronchioles belong to the respiratory unit

Respiratory unit
Respiratory bronchioles Alveolar ducts Alveolar sacs Alveolus

The respiratory Acinus


The respiratory membrane is composed of two epithelial cells 1.The type 1 pneumocyte- most abundant, thin and flat. This is where gas exchange

occurs

2. The type 2 pneumocyte- secretes the lung surfactant Surfactant:


Surface active agent Detergent 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 Pleura
Surrounds the lungs and provide protection 1. Parietal pleura- in the chest wall 2. Visceral pleura- intimately attached to the lungs 3. Pleural space- in between the two pleurae

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 cavity Hemothorax- Blood in the cavity ___________- Pus in the cavity ___________- Lymph in the cavity

CLINICAL Correlation: Pleural Effusion


Hydrothorax- Serous fluid in the pleural cavity Hemothorax- Blood in the cavity Pyothorax/Empyema- Pus in the cavity ________- Lymph in the cavity

CLINICAL Correlation: Pleural Effusion


Hydrothorax- Serous fluid in the pleural cavity Hemothorax- Blood in the cavity Pyothorax- Pus in the cavity Chylothorax- Lymph in the cavity

CLINICAL Correlation: Pneumothorax


Accumulation of air in the pleural space

The RIB CAGE

MECHANICS OF BREATHING
A. Muscles of Inspiration 1. 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 muscles a. Sternocleidomastoid muscles b. Scalene c. Pectoralis minor

Muscles of Expiration 1. 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 nerve During INSPIRATION, it contracts downwards During EXPIRATION, it relaxes and moves upwards

Respiratory Muscles

Respiratory Physiology
1. Ventilation and gas exchange 2. Mechanics of breathing 3. Gas transport 4. Pulmonary volumes and capacities 5. Respiratory control

OXYGEN moves by the mechanism of DIFFUSION Exchange of gases across the respiratory membranes is influenced by: 1. Thickness of the membrane e.g. pulmonary edema thickness doubled > decreased rate of diffusion 2. Total surface area e.g. emphysema and lung Ca > restricted gas exchange 3. Concentration gradient for gases across the membrane.

Gas exchange

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 Pressures
Major factors in determining the extent of lung expansion and compliance during the processes of inspiration and expiration:
Alveolar pressure Intrapleural pressure Alveolar surfactant

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

Pulmonary Pressures
Boyles 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 Pressures
Boyles 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 Pressures
Intrapleural 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 Pressures
Surfactant:
Surface active agent Detergent that greatly decreases the surface tension of fluid lining the alveoli.

Ventilation
Ventilation is the movement of air into the lungs

Fig. 15.11a

Fig. 15.11b

Control of Respiration: Central


Respiratory center in the medulla Controls the rate and depth of respiration Increased 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 O2 Decreased O2 (HYPOXIA) increase respiration Decreased pH (acidosis) increase respiration

2. Hering-Breurer reflex
Stretch 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 Reflex


Irritant 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


Motor signals are transmitted back to the respiratory system.

Respiratory muscles contract rapidly generating high pressures in the lungs while the vocal cords remain tightly closed.

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

The Sneeze Reflex


Irritant 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


Motor signals are generated and transmitted back.

Respiratory muscles contract rapidly generating high pressures in the lungs while the vocal cords remain tightly closed.

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

Cough and sputum production


Cough is a protective reflex Sputum production has many stimuli Thick, yellow, green or rustcolored bacterial pneumonia Profuse, Pink, frothy pulmonary

edema
tumor

Scant, pink-tinged, mucoid Lung

Cough Find 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 worse Determine how long it has been present and has there been any change in its characteristics

Sputum The 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: Scant Copious

Consistency: Thick Viscous Frothy Mucoid Watery Mucopurulent Cast

Symptoms of Pulmonary Disease


Persistent cough
Always abnormal Chronic 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


Intervention 1. Provide adequate hydration 2. Administer aerosolized solutions 3. advise smoking cessation 4. 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

Cyanosis
Bluish discoloration of the skin

A LATE indicator of hypoxia


Appears when the unoxygenated hemoglobin is more than 5 grams/dL Central cyanosis observe color on the undersurface of tongue and lips Peripheral cyanosis observe the nail beds, earlobes

Cyanosis
Interventions:
Check for airway patency Oxygen therapy Positioning Suctioning Chest physiotherapy Measures to increased hemoglobin

Hemoptysis
Expectoration of blood from the respiratory tract Hemoptysis
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 emboli Bleeding from stomach acidic pH, coffee ground material

Hemoptysis Coughing 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


Hemoptysis Usually frothy Alkaline pH Hematemesis Never frothy Acidic pH

Hemoptysis
Interventions: Keep patent airway Determine the cause Suction and oxygen therapy Administer Fibrin stabilizers like aminocaproic acid and tranexamic acid

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

Origin Chest wall

Characteristics Well-localized constant ache increasing with movement Sharp, abrupt onset increasing with inspiration or with sudden ventilatory effort (cough, sneeze), unilateral

Possible Causes Trauma, cough, herpes zoster

Pleura

Lung Parenchyma

Dull, constant ache, poorly localized

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

Epistaxis
Bleeding from the nose caused by rupture of tiny, distended vessels in the mucus membrane A vast network of capillaries, called Kiesselbachs plexus, line the mucosa of the nasal cavity. Most common site- anterior septum Causes: 1. trauma 2. infection 3. Hypertension 4. 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.

Epistaxis
Interventions 1. Position patient: Upright, leaning forward, tilted prevents swallowing and aspiration 2. Apply direct pressure. Pinch nose against the middle septum x 5-10 minutes 3. If unrelieved, administer topical vasoconstrictors, silver nitrate, gel foams 4. Assist in electrocautery and nasal packing for posterior bleeding

Acute Respiratory Failure


Sudden and life-threatening deterioration of the gas-exchange function of the lungs
Occurs when the lungs no longer meet the bodys metabolic needs

Acute Respiratory Failure


Defined clinically as:

1. PaO2 of less than 50 mmHg


2. PaCO2 of greater than 50 mmHg 3. Arterial pH of less than 7.35

Acute Respiratory Failure


CAUSES CNS depression- head trauma, sedatives CVS diseases- MI, CHF Airway irritants- smoke, fumes Endocrine and metabolic disordersmyxedema, metabolic alkalosis Thoracic abnormalities- chest trauma

Acute Respiratory Failure


PATHOPHYSIOLOGY

Decreased Respiratory Drive


Brain injury, sedatives, metabolic disorders impair the normal

response of the brain to normal respiratory stimulation

Acute Respiratory Failure


PATHOPHYSIOLOGY

Dysfunction 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


PATHOPHYSIOLOGY Dysfunction of the Lung Parenchyma Pleural effusion, hemothorax, pneumothorax, obstruction interfere ventilation prevent lung

expansion

Acute Respiratory Failure


ASSESSMENT FINDINGS

Restlessness

Dyspnea Cyanosis Altered respiration Altered mentation Tachycardia Cardiac arrhythmias Respiratory arrest

Acute Respiratory Failure


DIAGNOSTIC FINDINGS

Pulmonary function test ABG=pH below 7.35 CXR- pulmonary infiltrates ECG- arrhythmias

Acute Respiratory Failure


MEDICAL TREATMENT

Intubation Mechanical ventilation


Antibiotics Steroids Bronchodilators

Acute Respiratory Failure


INTERVENTIONS
1. Maintain patent airway 2. Administer O2 to maintain Pa02 at more than 50 mmHg 3. Suction airways as required 4. Monitor serum electrolyte levels 5. Administer care of patient on mechanical ventilation

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

COPD
Asthma Chronic bronchitis Emphysema Bronchiectasis

COPD: risk factors


The most common cause of COPD is cigarette smoking. Others- fumes, air pollution

COPD
The general pathophysiology In COPD there is airflow limitation that is both progressive and associated with abnormal inflammatory response of the lungs

ASTHMA
The acute episode of airway obstruction is characterized by

airway hyperactivity to various stimuli

Asthma Pathophysiology
Immunologic/allergic reaction results
three main airway responses a. Edema of mucous membranes b. Spasm of the smooth muscle of
in histamine release, which produces

bronchi and bronchioles c. Accumulation of tenacious secretions

Asthma Assessment Findings


Assessment findings: history

1. Family history of allergies 2. Client history of eczema

Assessment findings
Respiratory distress

Asthma Assessment Findings

Shortness of breath Expiratory wheeze Use of accessory muscles Irritability diaphoresis, cough, anxiety, weak pulse

Emphysema
There 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 asthma Aging process Disequilibrium between ELASTASE & ANTIELASTASE (alpha-1-antitrypsin)

Destruction of distal airways and alveoli Overdistention 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. Dyspnea 5. Barrel chest

Emphysema Assessment
Hyper-resonance in percussion, decreased breath sounds with prolonged expiration Diagnostic tests: pCO2 elevated,

PO2 normal or slightly decreased

Chronic bronchitis
Chronic 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 rhonchi 2. Feeling of epigastric fullness, cyanosis, distended neck veins,

edema

3. 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 loss 3. Diagnostic tests
Bronchoscopy reveals sources and sites of secretions

COPD Asthma Emphysema Bronchitis

Major Pathophysiology Bronchial hypersensitivity Distal airway DESTRUCTION Hyper-secretion of Mucus and inflammation

Major Manifestation

COPD

Wheezing (reversible) BARREL CHEST and thin body Abundant mucopurulent sputum and cough, Cor pulmonale Hemoptysis and infection

Bronchiectasis Chronic destruction of bronchus

COPD Management
1. Rest- To reduce oxygen

demands of tissues

2. Increase fluid intake- To

liquefy mucus secretions sputum and prevent infection

3. Good oral care- To remove

COPD Management
4. Diet

High caloric diet provides source of


energy

High protein diet helps maintain


integrity of alveolar walls

Moderate fats Low carbohydrate diet limits carbon dioxide production (natural end product).

COPD Management
5. 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 Management
6. Avoid cigarette smoking, alcohol, and environmental pollutants.
7. CPT percussion, vibration, postural drainage

COPD Management
8. Bronchial hygiene measures Steam inhalation Aerosol inhalation

COPD Management
Pharmacotherapy 1. Expectorants (guaiafenessin)/ mucolytic (mucomyst/mucosolvan) 2. Antitussives Dextrometorphan Codeine

COPD Management
Pharmacotherapy

3. Bronchodilators
Aminophylline (Theophylline) Ventolin (Salbutamol) Bricanyl (Terbutaline) Alupent (Metaproterenol)
Observe for tachycardia

Bronchodilators
Types Beta 2 agonists Examples Salbutamol Terbutaline Aminophylline Theophylline Ipratropium Action Stimulate Beta 2 receptor in bronchus Relaxes bronchial smooth muscle Blocks parasympathetic system

Direct Bronchodilator
Anti-cholinergic

COPD Management
Pharmacotherapy 4. Antihistamine Benadryl (Diphenhydramine) Observe for drowsiness
5. Steroids Anti-inflammatory effect 6. Antimicrobials

Oxygenation

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