Post on 10-Sep-2014
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
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!!!