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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…