Respiratory system

and Its diseases

Submitted By: Constante,

Quolette M.BSN IV-B NCM 104

Submitted to:Mr. Carlo Hidalgo

Primary Function

The exchange of gases between the environmental air and the blood.– Ventilation– Diffusion– Perfusion

Nonrespiratory Functions of the Respiratory System Water loss and heat elimination Warms and humidifies inspired air Enhances venous return Contributes to normal acid-base balance Enables speech, singing, etc. Defends against inhaled foreign matter. Removes, modifies, activates various materials passing

through the pulmonary circulation. Inactivates prostaglandins Activates angiotensin II

Nose - organ of smell

Structure of the Respiratory System

Respiratory airways– Nasal passages– Pharynx– Trachea– Bronchi– Bronchioles

Lungs - left lung - 2 lobes; right lung - 3 lobes– Alveoli• Type I alveolar cells• Type II alveolar cells• Alveolar macrophages• Pores of Kohn

Alveolar fluid liningwith pulmonary surfactant

Type II alveolar cell

Type I alveolar cell

Interstitial fluid

Alveolus

Alveolarmacrophage

Erythrocyte

Pulmonarycapillary

Lungs, contd.– Pulmonary capillaries– Elastic connective tissue– Pleural sac

Thorax

Respiratory Mechanics Air moves from an area of high pressure to an

area of low pressure, following the pressure gradient.

Pressure considerations–Atmospheric pressure– Intra-alveolar pressure– Intrapleural pressure

Major Inspiratory Muscles

Quiet breathing–Diaphragm– External intercostal muscles

Deeper inspirations–Accessory inspiratory muscles

ExpirationExpiration is normally a passive process.

Inspiratory muscles relaxChest wall and lungs recoilIntra-alveolar pressure increasesAir leaves the lungs For more complete and rapid emptying:– Abdominal muscles– Internal intercostal muscles

Airway Resistance

Bronchoconstriction - parasympathetic stimulation

Bronchodilation - sympathetic stimulation

Lung Elasticity

Elastic recoil and compliance–Connective tissue –Alveolar surface tension

Pulmonary Surfactant

Secreted by Type II alveolar cellsReduces alveolar surface tension– Increased pulmonary compliance– Reduces the lungs tendency to recoil

Energy Expenditure is Increased When:

Pulmonary compliance is decreasedAirway resistance is increasedElastic recoil is decreasedThere is need for increased ventilation

Lung Volumes

• Normal range:–Male - 5.7 liters–Female - 4.2 liters•500 ml of air are inspired and

expired•At end of quiet expiration, the lungs

still contain 2,200 ml of air

Gas exchange continues during expiration–Maintains constant gas content–Decreased energy utilization

Tidal volumeResidual volumeVital capacityTotal lung capacityForced expiratory volume in one second

Alveolar Ventilation

Pulmonary ventilationRespiratory RateAnatomical dead spaceAlveolar ventilationAlveolar dead space

Local Regulation

• Goal - Maximally match blood flow to airflow

¯ Airflow in comparison to blood flow CO2 relaxation of airway airflow

blood flow in comparison to air flow O2 in alveolus and surrounding tissues vasoconstriction of pulmonary arteriole blood flow

Gas Exchange

Simple diffusion down partial pressure gradients

Partial Pressure The individual pressure exerted independently by a

particular gas within a mixture of gases. The air we breath exerts a total atmospheric pressure

of 760 mm Hg (at sea level) and is composed of:– 79% Nitrogen - PN2 = 760 mm Hg x .79 - 600 mm

Hg– 21% Oxygen - PO2 = 760 mm Hg x .21 = 160 mm Hg

– The partial pressure of CO2 is negligible at 0.03 mm Hg

Amount of gas that dissolves in blood depends on:Solubility of the gas in bloodPartial pressure of the gas

The difference in partial pressure between pulmonary blood and alveolar air is known as a partial pressure gradient.

Alveolar Air

Inspired air is humidified - water vaporFresh inspired air mixes with the large volume

of old air and the dead space - at the end of each inspiration, less than 15% of the air in the alveoli is fresh air.

The average alveolar PO2 is 100 mm Hg.

O2 and CO2 Exchange

Only small fluctuations occur in alveolar PO2 throughout both inspiration and expiration.– Small proportion of total air exchanged– Oxygen rapidly moves down its partial pressure

gradient

–Pulmonary blood PO2 equilibrates with alveolar PO2

–PO2 of arterial blood is fairly constant

O2 and CO2 Exchange – Alveoli Level

Alveolar PCO2 also remains fairly constant at 40 mm Hg.

Partial pressures of gases favor the movement of O2 from the alveoli into the blood and CO2 from the blood into the alveoli.

O2 and CO2 Exchange

O2 uptake matches O2 use even when O2 consumption increases due to increased metabolism.

Rate of Diffusion

Surface areaThickness of the membraneDiffusion coefficient of the particular gas.

These factors are relatively constant under resting conditions, therefore the partial pressure is the primary factor that determines rate of exchange.

O2 and CO2 Exchange – Tissue Level

Partial pressures of gases favor the movement of O2 from the blood into the adjacent cells and CO2 from the cells into the capillary blood.

Gas Transport

Oxygen– Dissolved oxygen (1.5%)– Chemically bound to hemoglobin (98.5%)

The PO2 of the blood is a measurement only of the dissolved oxygen.

Hemoglobin

Four polypeptide chainsFour iron-containing heme groups that are

able to combine with an O2 molecule.

If Hb is carrying its maximum O2 load, it is considered to be fully saturated.

Storage for oxygenMaintains a low PO2

At the tissue level, as the PO2 falls the Hb unloads some of its stored oxygen.

Oxyhemoglobin Dissociation Curve

Plateau portion–Range that exists at the pulmonary

capillaries.

Note: Minimal reduction of oxygen transported until the PO2 falls below 60 mm Hg.

Steep portion of the curve–Range that exists at the systemic

capillaries

A small drop in systemic capillary PO2 can result in the release of large amounts of oxygen for the metabolically active cells.

Factors that Affect the Binding of Hemoglobin and Oxygen

Carbon dioxideAcidity Temperature

Bohr effect – Reduction in the affinity of hemoglobin for oxygen in response to an increase in blood carbon dioxide and a decrease in pH.

Gas Transport

Carbon Dioxide– Dissolved CO2 (10%)– Carbamino hemoglobin (30%)– Bicarbonate (60%)– Chloride shift

Haldane effect – the ability of hemoglobin to pick up CO2 and CO2-generated H+.

Control of Respiration

Neural controlChemical stimuli

Neural Control

Respiratory control centers housed in the brain stem– Inspiratory and expiratory neurons in the

medullary respiratory center• Dorsal respiratory group• Ventral respiratory group• Rostral ventromedial medulla

Respiratory control centers housed in the brain stem, contd.– Apneustic– Pneumotaxic center

Stretch receptors in the lung (Hering Breuer reflex)– Prevents overinflation of the lung

Ventilation is matched to the body’s needs for oxygen uptake and carbon dioxide removal–Medullary respiratory center receives input–Appropriate signals sent to motor neurons–Rate and depth of ventilation adjusted

Chemical Stimuli

Arterial PO2

Arterial PCO2

Arterial H+

Arterial PO2

Monitored by peripheral chemoreceptorsPO2 must fall below 60 mm Hg to stimulate

increased respirationPeripheral chemoreceptors respond to the PO2

and not the total oxygen content.

Major regulator of ventilation under resting conditions.

CO2 crosses the blood-brain barrier forming H+

Arterial H+

Monitored by aortic and carotid body peripheral chemoreceptors

Plays a role in adjusting ventilation in response to alterations in arterial H+ concentrations unrelated to fluctuations in PCO2

Diagnosis of Pulmonary Function

Clinical Assessment

Symptoms of Pulmonary Disease

Dyspnea– Sensation of breathlessness that is excessive for any given

level of physical activity. Paroxysmal nocturnal dyspnea– Inappropriate breathlessness at night.

Orthopnea– Dyspnea on recumbency.

Platypnea– Dyspnea on the upright position relieved by recumbency.

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.

Stridor– Crowing sound during breathing.– Caused by turbulent airflow through a narrowed upper

airway.– Inspiratory stridor implies extratracheal variable airway

obstruction.– Expiratory stridor implies intratracheal variable airway

obstruction.– Stertorous breathing is an inspiratory sound due to

vibration in the pharynx during sleep.

Wheezing– Continuous musical or whistling noises caused by

turbulent airflow through narrowed intrathoracic airways.– Most, but not all, are due to asthma.

Hemoptysis– Expectoration of blood.– Often the first indication of serious bronchopulmonary

disease.– Massive hemoptysis: coughing up of more than 600 ml of

blood in 24 hours.

Signs of Pulmonary Disease Tachypnea– Rapid, shallow breathing.– Arbitrarily defined as a respiratory rate in excess of

18/min. Bradypnea– Slow breathing.

Hyperpnea– Rapid, deep breathing.

Hyperventilation– Increase in the amount of air entering the alveoli.

Kussmaul respiration (air hunger)– Deep, regular sighing respiration, whether the rate be normal

slow or fast.– Occurs in diabetic ketoacidosis and uremia, as an exaggerated

form of bradypnea. Cheyne-Stokes respiration

– Commonest form of periodic breathing.– Periods of apnea alternate regularly with series of respiratory

cycles. In each series, the rate and amplitude increase to a maximum followed by cessation.

Biot breathing– Uncommon variant of Cheyne-Stokes respiration.– Periods of apnea alternate irregularly with series of breaths of

equal depth that terminate abruptly.– Most often seen in meningitis.

Singultus– Sudden, involuntary diaphragmatic contraction producing

an inspiration interrupted by glottal closure to emit a characteristic sharp sound.

– Causes:• Reflex stimulation without organic disease• Diseases of the central nervous system• Mediastinal disorders• Pleural irritation• Abdominal disorders• Diaphragmatic stimulation

Physical chest deformitiesThe thorax is usually symmetric, both sides rise equally on

inspiration.Chest asymmetry at rest:

• Scoliosis• Chest wall deformity• Severe fibrothorax

Conditions with unilateral loss of lung volumeSymmetrically reduced chest expansion during deep

inspiration:• Neuromuscular disease• Emphysema• Ankylosis of the spine

Asymmetric chest expansion during inspiration:• Unilateral airway obstruction• Pleural or pulmonary fibrosis• Splinting due to chest pain• Pleural effusion• Pneumothorax

Expansion on the chest, collapse of the abdomen on inspiration:• Weakness or paralysis of the diaphragm

Chest collapse, rise of the abdomen on inspiration:• Airway obstruction• Intercostal muscle paralysis• Flail deformity of the chest

Pulsus paradoxicusThe arterial blood pressure normally falls about 5 mmHg to a

maximum of 10 mmHg on inspiration.Exaggeration of the normal response.Seen in:

• Severe asthma or emphysema• Upper airway obstruction• Pulmonary embolism• Pericardial constriction or tamponade• Restrictive cardiomyopathy

CyanosisBluish discoloration of skin or mucous membranes.Caused by increased amounts (>5 g/dL) of unsaturated /

reduced hemoglobin.Presents as either central or peripheral cyanosis

Digital clubbingAnteroposterior thickness of the index finger at the base of the

fingernail exceeds the thickness of the distal interphalangeal joint.

Helpful clues:• Nail bed sponginess• Excessive rounding of the nail plate• Flattening of the angle between the nail plate and the proximal nail skin

fold

Percussion sounds (resonance, dullness, hyperresonance) Auscultatory sounds (vesicular, bronchial,

bronchovesicular) Adventitious sounds

Abnormal sounds on auscultationMay be classified as continuous (wheezes, rhonchi) or

discontinuous (crackles, crepitations)

Wheezes– High-pitched sounds which results from bronchospasm,

bronchial or bronchiolar mucosal edema, or airway obstruction by mucus, tumors, or foreign bodies.

Rhonchi– Low-pitched sounds caused by sputum in large airways and

frequently clear after coughing. Crackles

– Generated by the snapping open of small airways during inspiration.

– Fine crackles are heard in interstitial diseases, early pneumonia or pulmonary edema, patchy atelectasis and in some patients with asthma or bronchitis.

– Coarse crackles are heard late in the course of pulmonary edema or pneumonia.

FremitusVoice vibrations on the chest wall.Localized reduction in fremitus occurs over areas of air or fluid

accumulation in the lungs. Increased fremitus suggests lung consolidation.

Bronchophony Increased intensity and clarity of the spoken word during

auscultation.Heard over areas of consolidation or lung compression.

Whispered pectoriloquyExtreme form of bronchophony in which softly spoken words are

readily heard by auscultation. Egophony

Auscultation of an “a” sound when the patient speaks an “e” sound.

TYPICAL CHEST EXAMINATION FINDINGS IN SELECTED CLINICAL CONDITIONS

CONDITION PERCUSSION FREMITUS BREATH SOUNDS

VOICE TRANSMISSION

ADVENTITIOUS SOUNDS

Normal Resonant Normal Vesicular Normal Absent

Consolidation or Atelectasis (with patent airway)

Dull Increased Bronchial Bronchophony, whispered

pectoriloquy, egophony

Crackles

Consolidation or Atelectasis (with blocked airway)

Dull Decreased Decreased Decreased Absent

Bronchial Asthma

Resonant Normal Vesicular Normal Wheezing

Diagnosis of Pulmonary Function

Laboratory Assessment

Routine Radiography Integral part of the diagnostic evaluation of diseases

involving the pulmonary parenchyma, the pleura, and to a lesser extent, the airways and the mediastinum.

Usually involves a postero-anterior view and a lateral view.

Lateral decubitus views are often useful for determining whether pleural deformities represent freely flowing fluid.

Apicolordotic views visualize disease at the lung apices better than the standard posteroanterior view.

Chest Radiography

Ultrasonography

Not useful for evaluation of the pulmonary parenchyma.

Helpful in the detection and localization of pleural fluid.

Computed Tomography

Offers several advantages over conventional radiographs.

Use of cross-sectional images makes it possible to distinguish between densities.

Better at characterizing tissue densities and providing accurate size of lesions.

Magnetic Resonance Imaging

Pulmonary Function Tests

Objectively measure the ability of the respiratory system to perform gas exchange by assessing ventilation, diffusion and mechanical properties.

Composed of the spirometry test and ventilation-perfusion (V/Q) test.

Indications:Evaluation of the type and degree of pulmonary

dysfunction (obstructive or restrictive)Evaluation of dyspnea, cough and other symptomsEarly detection of lung dysfunctionSurveillance in occupational settingsFollow-up or response to therapyPreoperative evaluationDisability assessment

Relative contraindications:Severe acute asthma or respiratory distressChest pain aggravated by testingPneumothoraxBrisk hemoptysisActive tuberculosis

Spirometry– Allows for the determination of the presence and severity

of obstructive and restrictive pulmonary dysfunction.– The hallmark of obstructive pulmonary dysfunction is

reduction of airflow rates.– Restrictive pulmonary dysfunction is characterized by

reduction in pulmonary volumes.

Diseases of the Respiratory System

Nose, Paranasal Sinuses and Larynx

Influenza

Influenza viruses, members of the Orthomyxoviridae family, include types A, B and C.

Outbreaks occur virtually every year and communicability is influenced by antigenic shifts and viral mutations that “confuse” the affected patient’s immune system.

Clinical Manifestations

Incubation period of 3-6 days. Acute illness usually resolves over 2-5 days. Most patients largely recover within 1 week. Symptoms and Signs:

Abrupt onset of headacheFever and chillsMyalgia and malaiseCough, sneezing and sore throat

The major problem posed consists of its complications:Primary influenza viral pneumoniaSecondary bacterial pneumoniaMixed viral and bacterial pneumoniaExtrapulmonary complications:

• Reye’s syndrome• Myositis, rhabdomyolysis and myoglobinuria• Encephalitis, transverse myelitis• Guillain-Barré syndrome

Treatment Treatment for uncomplicated influenza is symptomatic

Salicylates should be avoided in children because of its association with Reye’s syndrome.

Increased oral fluid intake.Ascorbic acid

Antivirals:Amantadine (Influenza A)Rimantadine (Influenza B)Ribavirin (Influenza A and B)

Prophylaxis:– Vaccination against Influenza A and B– Amantadine and rimantadine

Viral Rhinitis The nonspecific symptoms of the ubiquitous common

cold are present in the early phases of many diseases that affect the upper aerodigestive tract.

Rhinoviruses, members of the Picornaviridae family, are a prominent cause of the common cold, with seasonal peaks in the early fall and spring.

Infections highest among infants and young children and decrease with age.

The infection is spread by contact with infected secretions or respiratory droplets or by hand-to-hand contact, with autoinoculation of the conjunctival or nasal mucosa.

Clinical Manifestations

Incubation period of 1 to 2 days. Illness generally lasts 4 to 9 days and resolves

spontaneously. Symptoms:

HeadacheNasal congestionWater rhinorrheaSneezingScratchy throatGeneral malaise and occasionally fever

Signs:Reddened, edematous nasal mucosaWater nasal discharge

Rhinoviruses are not a major cause of lower respiratory tract disease.

Rhinoviruses may cause exacerbations of asthma and chronic pulmonary disease in adults.

Complications:Transient middle ear effusionSecondary bacterial infection

Because of the mild nature and short duration of the illness, a specific diagnosis is not commonly needed; however, viral cultures can be performed.

Treatment

No proven specific treatment. Supportive measures:

Decongestants should not be used for more than a week because of rebound congestion noted after cessation (rhinitis medicamentosa).

AntipyreticsLiberal fluid intakeAscorbic acid

Other Viral URTI:CoronavirusAccount for 10 to 20% of common colds.Most active in late fall, winter and early spring

– a period when the rhinovirus is relatively inactive.

Symptoms are similar to those of rhinovirus, but the incubation period is longer (3 days) and usually lasts 6 to 7 days.

Mutations of the virus brought about the SARS phenomenon.

Other Viral URTI:Respiratory Syncytial VirusBelongs to the Paramyxoviridae family.Major respiratory pathogen of young children

and is the foremost cause of lower respiratory disease in infants.

Transmitted by close contact with fingers or fomites as well as through coarse (not fine) aerosols produced by coughing or sneezing.

Incubation period of 4 to 6 days.Viral shedding may last two weeks in children

but is much shorter in adults.

Clinical Manifestations:RhinorrheaLow-grade feverMild systemic symptoms Cough and wheezing25-40% with lower respiratory tract involvement

Treatment:Antiviral ribavirin for children and infants.No specific treatment for adults.

Other Viral URTI:Parainfluenza Virus Single-stranded RNA virus of the Paramyxoviridae

family. Important cause of mild illnesses and croup

(laryngotracheobronchitis), bronchiolitis and pneumonia.

Clinical Manifestations:Cold or hoarseness with coughAcute febrile illness with coryzaBarking cough and frank stridor in children

Treatment:– In mild illness, treatment is symptom-based.– Mild croup may be treated with moisturized air

from a vaporizer.– More severe cases require hospitalization and

close observation for development of respiratory distress.

– No specific antiviral treatment is available.

Other Viral URTI:Adenovirus Infections occur frequently in infants and children

with a seasonal distribution of fall to spring.Certain serotypes are associated with outbreaks

of acute respiratory disease in military recruits.Transmission can take place via inhalation of

aerosolized virus, through the inoculation of the conjunctival sac, and probably by the fecal-oral route.

Clinical Manifestations:RhinitisPharyngoconjunctival fever (bilateral conjunctivitis, low-

grade fever, rhinitis, sore throat and cervical lymphadenopathy)

In adults, the most frequent syndrome is the acute respiratory disease seen in military recruits, with prominent sore throat, fever on the second or third day of illness, cough, coryza and regional lymphadenopathy.

Diagnosis and Treatment:Diagnosis is established by isolation of the virus.No specific antiviral therapy is available.A live oral vaccine is available and used widely to prevent

outbreaks among military recruits.

Acute Bacterial Sinusitis Symptoms of rhinitis plus clinical signs and

symptoms that indicate involvement of the affected sinus or sinuses such as pain and tenderness over the involved sinus.

Occurs when an undrained collection of pus accumulates in a sinus.

Typical Pathogens:– Streptococcus pneumoniae– Other streptococci– Haemophilus influenzae– Staphylococcus aureus– Moraxella catarrhalis

Signs and Symptoms:Pain on pressure over the cheeks (maxillary sinuses are the

most common sinuses affected).Discolored nasal discharge and poor response to

decongestants.Headache “in the middle of the head” or in the forehead.

Imaging:TransilluminationCaldwell view (frontal)Waters view (maxillary)Lateral view (sphenoid)Submentovertical view (ethmoid)CT scan for recurrent sinusitisMRI if malignancy in suspected

Treatment

Uncomplicated:Outpatient managementOral decongestants and nasal decongestant spraysAppropriate oral antibiotics for at least two weeks * Amoxicillin provides better sinus

penetration than ampicillin. Complicated:

Failure of sinusitis to resolve after a completed course of antibiotic treatment.

Hospitalization for intravenous antibiotics.

Complications:– Lower respiratory tract infections– Osteomyelitis and mucocoele– Intracranial complications– Malignancy (?)

Allergic Rhinitis

“Hay fever” Symptoms mimic that of viral rhinitis but more

persistent and show seasonal variation. Symptoms:

Watery rhinorrheaEye irritation, pruritus, erythema and tearing

Signs:Pale or violaceous turbinatesOccasional polyposis

Treatment

Symptomatic in most cases.Oral decongestantsAntihistaminesNasal corticosteroid spraysMaintaining an allergen-free environmentAir purifiers and dust filtersDesensitization

Epistaxis

Bleeding from Kiesselbach’s plexus Predisposing factors:

Nasal trauma (nose picking, foreign bodies, forceful nose blowing)

RhinitisDrying of the nasal mucosa from low humidityNasal septal deviationAlcohol useAntiplatelet medicationsBleeding diathesis

Treatment:Direct pressure on the bleeding site.Venous pressure is reduced in the sitting position, and

leaning forward lessens the swallowing of blood.Short-acting nasal decongestant spraysCauteryTreatment of other possible underlying causes of bleeding

Diseases of the Respiratory System

Diseases of the Airways

Asthma

Increased responsiveness of lower airways to multiple stimuli.

Episodic and with reversible obstruction.May range in severity from mild without

limitation of patient’s activity, to severe and life-threatening.

Men and women are equally affected.Afflicts children more commonly than adults.

Pathogenesis:Common denominator is nonspecific

hyperirritability of the tracheobronchial tree.Airway reactivity increased by:• Allergenic• Pharmacologic• Environmental, occupational• Infectious• Emotional• Activity-related

Signs and Symptoms:– Episodic wheezing– Chest tightness– Dyspnea and cough– Tachycardia and tachypnea with prolonged expiation– Ominous signs: fatigue, pulsus paradoxicus, diaphoresis,

inaudible breath sounds with diminished wheezing, inability to maintain recumbency, and cyanosis

Laboratory Findings:Increased WBC count with eosinophiliaViscid sputum on gross examinationCurschmann’s spirals on microscopic examination of

sputumCharcot-Leyden crystalsObstructive pattern on the pulmonary function testsDiminished peak expiratory flow rate (normal: 450-650

L/min in men; 350-500 L/min in women)Respiratory alkalosis and mild hypoxemia in ABGs.

Complications:ExhaustionDehydrationAirway infectionCor pulmonaleTussive syncopePneumothorax (rare)

Prevention:Comprehensive patient educationPharmacologic interventionEnvironment controlEarly treatment of chest infectionsRecognition and effective management of nasal

and paranasal disordersDiscontinuance of cigarette smokingPneumococcal and yearly influenza immunization

for patients with moderate to severe asthma

Classifications

Mild asthma:Intermittent brief symptoms up to two times weekly.Absence of symptoms between exacerbations.Brief symptoms with activity.Nocturnal symptoms less than twice a month.PEFR or FEV1 of 80% or more, with less than 20% variability

on exacerbations.

Moderate asthma:Symptoms more than one to two times weekly.Exacerbations affecting sleep and level of activity.Exacerbations lasting several days.Requirement for occasional emergency care.PEFR values 60-80% of predicted, with 20-30% variability

during exacerbations and greater than 30% on worst exacerbations.

Severe asthma:Continuous symptomsFrequent exacerbationsLimitations of physical activitiesFrequent nocturnal symptomsRequirement for frequent emergency carePEFR less than 60% of predicted, with variability of 20-30%

on treatment, and greater than 50% on severe exacerbations

Prolonged asthma refractory to conventional modes of therapy (status asthmaticus)

Treatment

Severe ambulatory asthma:Daily maintenance therapy with inhaled corticosteroidsDaily oral sustained-release theophylline or oral β2-agonist

drugsLong-acting inhaled β2-agonist drug (salmeterol)Inhaled anti-cholinergic drug (ipratropium bromide)Short-acting inhaled β2-agonist drug for breakthrough

wheezingOral steroids

Status asthmaticus:Supplemental oxygen, 1-3 L/minMonitoring with oximetryInhaled β2-agonist agentsIntravenous aminophyllineSubcutaneous terbutalineIntravenous corticosteroidsInhaled corticosteroidsOral corticosteroidsSupportive: hydration, physical therapy, MV

Prognosis

Outlook is excellent because of the availability of medications.

Better prognosis in those who develop asthma early in life.

Chronic Obstructive Pulmonary Disease (COPD) Characterized by airflow obstruction due to chronic

bronchitis or emphysema. Classifications:

Chronic Bronchitis• Excessive secretion of bronchial mucus.• Productive cough for 3 months or more in at least 2 consecutive

years.Emphysema

• Abnormal and permanent enlargement of air spaces distal to the terminal bronchiole, with destruction of their walls, and without obvious fibrosis.

EMPHYSEMA VS CHRONIC BRONCHITIS

EMPHYSEMA CHRONIC BRONCHITIS

HISTORY Onset of symptoms After age 50 After age 35

Dyspnea Progressive, constant, severe

Intermittent, mild to moderate

Cough Absent or mild Persistent, severe

Sputum production Absent or mild Copious

Sputum appearance Clear, mucoid Mucopurulent or purulent

Other features Weight loss“pink puffer”

Airway infections, right heart failure, obesity

“blue bloater”

EMPHYSEMA VS CHRONIC BRONCHITIS

EMPHYSEMA CHRONIC BRONCHITIS

CHEST X-RAY Bullae, blebs Present Absent

Overall appearance Decreased markings in the periphery

“Dirty lungs”

Hyperinflation Present Absent

Heart size Normal or small, vertical Large, horizontal

Hemidiaphragms Low, flat Normal, rounded

Causes:Cigarette smokingAir pollutionAirway infectionFamilial factorsAllergies

Symptoms and Signs:5th or 6th decade of lifeExcessive cough and sputum productionShortness of breath that have often been present

for 10 years or more Laboratory findings:

Secondary polycythemiaPresence of microorganisms in the sputumSpirometry shows obstructive patternHyperinflation on radiographs

Complications:Pneumonia and acute bronchitisPulmonary embolizationLeft ventricular heart failurePulmonary hypertensionChronic respiratory failureSpontaneous pneumothorax

Prevention:Smoking cessationEarly treatment of airway infectionsVaccination against pneumococcal pneumonia

and influenza.

Treatment:Discontinuance of cigarette smokingPatient educationRelief of bronchospasm• Ipratropium bromide• Maintenance therapy with oral theophylline• Oral corticosteroids

Aerosol therapyChest physiotherapyTreatment of complicationsHome oxygen therapy

Bronchiectasis

Permanent normal dilatation and destruction of bronchial walls.

May be caused by recurrent infection or inflammation.

Symptoms:– Chronic cough– Copious sputum production, often purulent– Hemoptysis– Recurrent pneumonia

Signs:Persistent crackles at the base of the lungs.Clubbing is infrequent.Copious foul-smelling sputum that separates into three

layers in a cup. Laboratory findings:

Crowded bronchial markings on chest x-ray.Small cystic spaces near the bronchi on chest CT scan.

Treatment:AntibioticsDaily chest physiotherapy with postural drainage and chest

percussionInhaled bronchodilatorsSurgical resectionDiagnostic and therapeutic bronchoscopy

Complications:Cor pulmonaleAmyloidosisVisceral abscesses at distant sites like the brain

Diseases of the Respiratory System

Lower Respiratory Tract Infections

Community-Acquired Pneumonia

Major health problem despite the availability of potent antimicrobial drugs.

Symptoms and Signs:– Fever and shaking chills– Purulent sputum production– Consolidation on physical examination– Adventitious breath sounds on auscultation

Pathophysiology

Laboratory findings: LeukocytosisPatchy infiltrates on chest radiographs “Atypical pneumonia” – clinico-radiographic dissonance;

often caused by Mycoplasma or Chlamydia pneumoniae; less striking symptoms and physical findings with non-purulent sputum production and absence of leukocytosis despite significant infiltrates on chest radiography; OR severe symptoms in the absence of significant radiographic findings

ManagementGuidelines for Management:

Criteria for hospitalization:• Age over 65 years old• Co-existing illness• Alteration in vital signs• Leukopenia or marked

leukocytosis• Respiratory failure• Septic appearance• Absence of supportive care at

home

Prevention:Pneumococcal vaccineInfluenza vaccine

Most common pathogens:Out-patient, without co-morbidity, < 60 years old• Streptococcus pneumoniae• Mycoplasma pneumoniae• Respiratory viruses• Chlamydia pneumoniae• Haemophilus influenzae• Legionella• Staphylococcus aureus• Mycobacterium tuberculosis

Most common pathogens:Out-patient, with co-morbidity, age > 60 years old

• Streptococcus pneumoniae• Respiratory viruses• Haemophilus influenzae• Moraxella catarrhalis

Hospitalized patients with CAP• Streptococcus pneumoniae• Haemophilus influenzae• Legionella• Staphylococcus aureus• Chlamydia pneumoniae

Treatment:

Should be directed towards the elimination of the suspected causative organism.

Respiratory supportIsolation from immunocompromised, or

potentially immunocompromised patients.

Hospital-Acquired Pneumonia

Essentials of Diagnosis:Occurs more than 48 hours after admission to the

hospital.One or more clinical findings (fever, cough,

purulent sputum) in most patients.Frequent in patients requiring intensive care and

mechanical ventilation.Pulmonary infiltrates on chest x-ray.

Most common pathogens:Pseudomonas aeruginosaStaphylococcus aureusEnterobacter sp.Klebsiella pneumoniaeEscherichia coli

Treatment:Empiric therapy must be started as soon as

pneumonia is suspected.Respiratory support

Pulmonary Tuberculosis

Infection beings when aerosolized droplets containing viable organisms are inhaled by a person susceptible to the disease.

Symptoms and Signs:Constitutional symptoms of fatigue, weight loss,

anorexia, low-grade fever, and night sweatsCoughPatients often appear chronically ill.Post-tussive apical rales.

Pathogenesis:After entry into the lungs in aerosolized droplets,

tubercle bacilli are ingested by macrophages and transported to regional lymph nodes, and from there, they disseminate widely.

Lesions are contained by a delayed-type hypersensitivity response (DTH; the tissue-damaging response), and the cell-mediated macrophage-activating response.

The development of host immunity and DTH is evidenced by acquisition of skin-test reactivity to tuberculin purified protein derivative (PPD).

Granulomatous lesions form and organisms survive within macrophages or necrotic material but do not spread further.

Reactivation may occur at a later time. In some cases, the immune response is inadequate to contain the infection, and symptomatic, progressive primary disease develops.

Laboratory findings

Recovery of Mycobacterium tuberculosis from cultures, or identification of organisms by DNA probe

Acid-fast bacilli in the sputumSerologic diagnosis by ELISAApical infiltrates on chest radiographsGhon and Ranke signsTuberculin skin test

Sputum examination for acid-fast bacilli (AFB) or direct microscopy is the most important diagnostic test to request for a patient clinically suspected to have PTB.

Sputum collection:Best obtained on three consecutive mornings.Clean and thoroughly rinse the mouth with water.Breathe deeply 3 times.After the third breath, cough hard and try to bring

up sputum from deep in the lungs.

Best obtained on three consecutive mornings.Clean and thoroughly rinse the mouth with water.Breathe deeply 3 times.After the third breath, cough hard and try to bring

up sputum from deep in the lungs.Expectorate the sputum into a sterile container

with a well-fitted cap.Collect at least 1 teaspoonful.Examine the specimen to see that it is not just

saliva. Repeat the process if necessary.

Supervised nebulization with a warm, sterile, hypertonic (3%) saline solution is useful for obtaining specimens from patients highly suspected of having PTB. It should be attempted for all cooperative patients who are smear-negative or unable to expectorate sputum spontaneously.

Sputum TB culture and sensitivity tests:Smear (-) patients with a strong clinical possibility

of PTB and suggestive chest x-rays.Smear (+) or (-) patients suspected of multi-drug

resistant PTB.Smear (+) patients demonstrating the “rise fall”

phenomenon.All cases of relapse.All cases of re-treatment.All cases of treatment failure.

PTB Classifications:Class I: exposure, no symptoms, no radiographic evidenceClass II: exposure, (+) symptoms, no radiographic evidenceClass III: active PTB; exposure, (+) symptoms, (+)

radiographic evidenceClass IV: treated PTBClass V: indeterminate

Treatment

Newly diagnosed PTB:At present, there is a lack of current evidence or

clear trends in favor of efficacy and superiority of 4 drugs over 3.

The use of four drugs daily in the intensive phase treatment adds an additional assurance against treatment failure should there be unexpected drug resistance and assuming adherence to the treatment regimen, also helps the loss of additional drugs.

Newly diagnosed PTB:Intensive Phase: 2HRZE(S)/4HR(E)• First 2 months: Isoniazid, Rifampicin,

Pyrazinamide and Ethambutol + Streptomycin (IM)• Next 4 months: Isoniazid and Rifampicin +

EthambutolMaintenance Phase: 3/6HR• Next 3 months: Isoniazid and Rifampicin• Check clinical profile. May discontinue after a

total of 9 months, or may continue as clinical evidence dictates.

Areas with high resistance rates:National Capital Region, including LagunaCebuDavaoZamboangaCavitePampanga

Areas with low resistance rates:PalawanMountain Province and Benguet

Empiric therapy for MDR-TB suspect:Use of at least some second-line drugs.Prescribe drugs which the patient has not

previously taken.The initial regimens should consist of at least

three drugs, preferably four or five, to which the bacilli are likely to be fully sensitive (injectable aminoglycoside and pyrazinamide, even if previously used, because resistance is usually unlikely).

Hospitalization is not necessary in most patients, but should be considered if the patient is incapable of self-care.

Preventive therapy:Should be given if the patient is under 35 years of

age with a positive tuberculin test (>10 mm) in the following conditions:• Foreign-born persons from countries with high

prevalence of TB.• Medically underserved, low-income groups• Residents of long-term care facilities

Preventive therapy:Isoniazid preventive therapy for 6 to 12 months.Vaccine:• BCG should be given to tuberculin-negative

persons.• Children who are repeatedly exposed to

individuals with untreated or ineffectively treated TB also benefit from BCG vaccination.

Diseases of the Respiratory System

Bronchogenic Carcinoma

Bronchogenic Carcinoma

Suspected etiologies:Cigarette smokingIonizing radiationAsbestosHeavy metalsIndustrial agentsLung scarsAir pollutionGenetic predisposition

Squamous cell carcinoma and adenocarcinoma are the most common types (30 to 35% of primary tumors each).

Small cell carcinoma and large cell carcinoma account for about 20 to 25% and 15% of cases, respectively.

10 to 25% of patients are asymptomatic, especially during the early course of the disease.

Initial Symptoms:CoughWeight lossDyspneaChest painHemoptysisChange in the patterns of the symptoms

Physical findings vary and may be totally absent:Superior vena cava syndromeHorner’s syndromePancoast’s syndromeRecurrent laryngeal nerve palsy with

diaphragmatic hemiparesisParaneoplastic syndromes

PARANEOPLASTIC SYNDROMES IN LUNG CANCER

CLASSIFICATION SYNDROME COMMON HISTOLOGIC TYPE

ENDOCRINE AND METABOLIC

Cushing’s syndrome Small cell

SIADH Small cell

Hypercalcemia Squamous cell

Gynecomastia Large cell

CONNECTIVE TISSUE AND OSSEOUS

Clubbing and hypertrophic pulmonary osteodystrophy

Squamous cell, large cell and adenocarcinoma

NEUROMUSCULAR Peripheral neuropathy Small cell

Subacute cerebellar degeneration Small cell

Myasthenia (Eaton-Lambert syndrome)

Small cell

Dermatomyositis All

PARANEOPLASTIC SYNDROMES IN LUNG CANCER

CLASSIFICATION SYNDROME COMMON HISTOLOGIC TYPE

CARDIOVASCULAR Thrombophlebitis Adenocarcinoma

Nonbacterial verrucous (marantic) endocarditis

Adenocarcinoma

HEMATOLOGIC Anemia All

Disseminated intravascular coagulation

All

Eosinophilia All

Thrombocytosis All

CUTANEOUS Acanthosis nigricans All

Erythema gyratum repens All

Laboratory findings:Cytologic examination of sputum permits

definitive diagnosis of lung cancer in 40 to 60% of cases.

CT scan and other imaging techniques. Treatment:

SurgeryChemotherapyRadiotherapyCombination therapyImmunomodulation

Prognosis:Over-all five-year survival rate is 10 to 15%.Determinants of survival:• Stage of disease at time of presentation• Patient’s general health• Age• Histologic type of tumor• Tumor growth rate• Type of therapy

Diseases of the Respiratory System

Ventilation and Perfusion Disorders

Pulmonary Thromboembolism

Pulmonary emboli arise from thrombi in the venous circulation or right side of the heart, from tumors that have invaded the venous circulation, or from other sources.

More than 90% originate as clots in the deep veins of the lower extremities.

Physiologic risk factors:Venous stasisVenous endothelial injuryHypercoagulability• Oral contraceptives• Cancer• Protein C or S deficiency• Antithrombin III deficiency

Clinical risk factors:Prolonged bed rest or inactivitySurgeryChildbirthAdvanced ageStrokeMyocardial infarctionCongestive heart failureObesityFractures of the hip or femur

Symptoms:Pleuritic chest pain (74%)Non-pleuritic chest pain (14%)Dyspnea (84%)Apprehension (59%)Cough (53%)Hemoptysis (30%)Sweats (27%)Syncope (13%)

Signs:Tachypnea (92%)Crackles (58%)Accentuated split second heart sound (53%)Tachycardia (44%)Fever > 37.8°C (43%)Phlebitis (32%)Diaphoresis (36%)Edema (24%)Murmur (23%)Cyanosis (19%)

Laboratory findings:Results of routine laboratory tests are not

helpful in diagnosing pulmonary thromboembolism.

Imaging and special examinations:• Chest radiography• Lung scanning• Venous thrombosis studies• Pulmonary angiography

Prevention:Critically importantIdentification of those at riskProphylaxis

Treatment:AnticoagulationThrombolytic therapyInferior vena cava filter

Prognosis:May cause sudden death.Depends on the underlying disease and on

proper diagnosis and treatment.Pulmonary hypertension may be a

complication.

Inhalation of Air Pollutants Clinical Findings:

Exposure to low levels is inconsequential.Exposure to high levels produces lower and upper

respiratory tract irritation. Treatment:

Healthy individuals exposed to the usual ambient levels of air pollution need not observe special precautions.

Patients with COPD or severe asthma should be advised to stay indoors and not engage in strenuous activity in areas of high pollution level.

Prognosis:Depends on the severity and type of

exposure.Also depends on the patient’s preexisting

pulmonary status.

MAJOR AIR POLLUTANTS, SOURCES AND ADVERSE EFFECTS

NOXIOUS AGENT SOURCES ADVERSE EFFECTS

OXIDES OF NITROGEN Automobile exhaust; gas stoves and heaters; wood-burning stoves; kerosene space heaters

Respiratory tract irritation, bronchial hyperreactivity, impaired lung defense, bronchiolitis obliterans

HYDROCARBONS Automobile exhaust, cigarette smoke

Lung cancer

OZONE Automobile exhaust, high altitude aircraft cabins

Cough, substernal discomfort, bronchoconstriction, decreased exercise performance, respiratory tract irritation

MAJOR AIR POLLUTANTS, SOURCES AND ADVERSE EFFECTS

NOXIOUS AGENT SOURCES ADVERSE EFFECTS

SULFUR DIOXIDE Power plants, smelters, oil refineries, kerosene space heaters

Exacerbation of asthma and chronic obstructive pulmonary disease, respiratory tract irritation, hospitalization may be necessary, and death may occur in severe exposure

Pulmonary Aspiration Syndromes Aspiration of inert materials:

May cause asphyxia if amount aspirated is massive.Most patients suffer no serious sequelae.

Aspiration of toxic materials:Results in clinically evident pneumonia.Treatment is supportive

“Café coronary”Acute obstruction of upper airways by food that occurs in

intoxicated individuals.Heimlich maneuver may be life-saving.

Retention of an aspirated foreign bodyChronic aspiration of gastric contentsMendelson’s syndrome

Disorders of Ventilation

Obesity-hypoventilation syndrome (Pickwickian syndrome)

Sleep-related breathing disordersObstructive sleep apneaHyperventilation syndrome

Acute Respiratory Failure

Clinical Findings:Signs and symptoms of the underlying diseaseHypoxemia and hypercapniaDyspnea is the chief symptom.CyanosisRestlessness, confusion, anxiety, deliriumTachypneaTachycardia, hypertension, cardiac arrhythmiasTremors

Treatment

Non-ventilatory respiratory support Ventilatory respiratory support

Tracheal intubation• Hypoxemia• Upper airway obstruction• Impaired airway protection• Poor handling of secretions• Facilitation of mechanical ventilation

Ventilatory respiratory supportMechanical ventilation• Apnea• Acute hypercapnia• Severe hypoxemia• Progressive patient fatigue

General supportive careNutritional supportMaintenance of fluid and electrolyte balancePsychological and emotional supportSkin care to avoid decubitus ulcersMeticulous avoidance of nosocomial infectionsPrevention of stress ulcers

Pleural Effusion

Essentials of Diagnosis:Asymptomatic in many cases; pleuritic chest pain

if pleuritis is present; dyspnea if effusion is large.Decreased tactile and vocal fremiti; dullness to

percussion; distant breath sounds; egophony if effusion is large.

Radiographic evidence of pleural effusion.Diagnostic findings on thoracentesis

Classifications:Exudative effusion (at least one of the following

features):• Pleural fluid protein to serum protein ratio > 0.5• Pleural fluid LDH to serum LDH ration > 0.6• Pleural fluid LDH greater than 2/3 of the upper

limit of the serum LDH.Transudative effusion• Very low protein content• Often seen in non-inflammatory states

Approach to ManagementPLEURAL EFFUSION

Perform diagnostic thoracentesisMeasure pleural fluid protein and LDH

Any of the following met?PF/serum protein > 0.5PF/serum LDH > 0.6PF LDH > 2/3 upper normal serum limit

EXUDATEFurther diagnostic procedures

TRANSUDATETreat CHF, cirrhosis, nephrosis

Yes No

EXUDATEFurther diagnostic procedures

Measure PF glucose, amylaseObtain PF cytologyObtain differential cell countCulture, stain PF

Amylase elevatedConsider: esophageal rupture,Pancreatic pleural effusionMalignancy

Glucose < 60 mg/dLConsider: MalignancyBacterial infectionsRheumatoid pleuritis

NO DIAGNOSIS

NO DIAGNOSIS

Consider pulmonary embolus(lung scan or pulmonary arteriogram)

Positive:Treat for PE

Needle biopsy ofpleura

Negative Positive: Treat for TB or CA

PPD

Negative

SYMPTOMS IMPROVINGNo: ConsiderThoracoscopy orOpen pleural biopsy

YesObserve

Positive: Treat for TB

Negative

Treatment:Treatment of the underlying conditionRemoval if the effusion is large (therapeutic

thoracentesis or tube thoracostomy)Pleurodesis

Pneumothorax Types:

SpontaneousTraumatic

Essentials of diagnosis:Acute onset of ipsilateral chest pain and dyspnea, often of

several days’ duration.Minimal physical findings in mild cases; unilateral chest

expansion, decreased tactile and vocal fremiti, hyperresonance, diminished breath sounds, mediastinal shift, cyanosis in tension pneumothorax.

Presence of pleural air on chest x-ray.

Treatment:Depends on the severity of the condition.Supportive and oxygen supplementation if

needed.Tube thoracostomy and pleurodesis.

Thank you…