respiratory
TRANSCRIPT
“Roses are red,
Violets are blue,
Without your lungs
Your blood would be, too.”
David D. Ralph, MDNew England Journal of Medicine
MEDICAL-SURGICAL NURSING
Arni A. Magdamo, MD, MHA, FPCP
University of the PhilippinesCollege of Medicine, College of Nursing
The Respiratory System
Normal Anatomy and Physiology
The Respiratory Process Respiration is the process by which
oxygen enters the body and is utilized by the cells for their metabolic processes. It essentially involves five interdependent steps.
Ventilation refers to the entry of air containing oxygen and other gases into the lungs.
The Respiratory Process Ventilation is followed by the diffusion
of gases from and into the alveoli and alveolar sacs. Oxygen from the alveoli passes through the respiratory membrane and enter the perialveolar capillaries, while carbon dioxide from the capillaries diffuses through the respiratory membrane to leave the lungs by means of exhalation.
The Respiratory Process Circulation makes it possible for oxygen
to reach the distant tissues, and for carbon dioxide to travel from the tissues back into the lungs.
The fourth component of the respiratory process involves another diffusion of gases, this time involving the entry of oxygen into target tissues, and the entry of carbon dioxide into the blood stream for delivery back into the lungs.
The Respiratory Process Cell metabolism and respiration are the
final steps of the respiratory process wherein oxygen is utilized by the cells, and carbon dioxide, along with other waste products, is produced.
The Upper Respiratory Tract:The Nose The bridge of the nose is bone, and most
of the external nose is cartilage. The nasal cavity houses one of the most
efficient filtering system of the body. The external nares is divided by the nasal
septum into right and left portions. The paranasal sinuses and the
nasolacrimal duct open into the nasal cavity.
Hairs inside the external nares trap debris.
The Upper Respiratory Tract:The Nose The nasal cavity is lined with
pseudostratified ciliated epithelium that traps debris and moves it to the pharynx.
The nasal turbinates or conchae provide for an additional filtering mechanism by creating a turbulent airflow within the nasal cavity that dislodges inhaled pollutants and make them adhere to the sticky mucosal surface of the nasal cavity.
The Upper Respiratory Tract:The Nose The superior part of the nasal cavity
contains the sensory cells for the sense of smell.
A vast network of capillaries, called Kiesselbach’s plexus, line the mucosa of the nasal cavity.
The Upper Respiratory Tract:The Nose
The Upper Respiratory Tract:The Pharynx The nasopharynx joins the nasal cavity
through the internal nares and contains the opening to the auditory (Eustachian) tube and the pharyngeal tonsils.
The oropharynx joins the oral cavity and contains the palatine and lingual tonsils.
The laryngopharynx opens into the larynx and the esophagus.
The Upper Respiratory Tract:The Pharynx
The Upper Respiratory Tract:The Larynx The larynx is a set of cartilages collectively
called the “voice box”. There are three unpaired cartilages. The
thyroid cartilage and cricoid cartilage form most of the larynx. The epiglottis covers the opening of the larynx during swallowing.
There are six paired cartilages. The corniculate, the arytenoid, and the cuneiform cartilages all serve as attachment sites on which the vocal cords are anchored.
The Upper Respiratory Tract:The Larynx The vocal cords are structures within
the larynx that vibrate to produce. There are two main groups.
The vocal folds are the true vocal cords, connective tissues that vibrate when air passes through them to produce the audible sound.
The Upper Respiratory Tract:The Larynx The vestibular folds are known as the
false vocal cords, because they merely serve as connective tissue support for the vocal folds.
The cords produce sounds of different pitches when their length is varied.
The Upper Respiratory Tract:The Trachea The trachea, also known as the “wind
pipe,” is a hollow tubular structure that connects the larynx to the lower respiratory organs (the respiratory tree).
It is a series of 15 to 20 C-shaped cartilages that are solid anteriorly, and supported posteriorly by a layer of smooth muscles which contract or relax to bring about dilation or constriction of the airways.
The Upper Respiratory Tract:The Trachea It is lined by pseudostratified ciliated
columnar epithelium which aids in the filtering of inhaled air.
The Upper Respiratory Tract:The Trachea
The Lower Respiratory Tract:The Respiratory Tree The primary bronchi extend from the
trachea to each lung. The right primary bronchus is shorter, wider and is oriented more vertically, while the left primary bronchus is longer, narrower and is oriented more horizontally.
There are two lungs. The right lung has three lobes and ten lobules, while the left lung has two lobes and nine lobules.
The Lower Respiratory Tract:The Respiratory Tree The airway passages of the lungs branch
and decrease in size. The primary bronchi form the secondary
bronchi, which go to each lobe of the lungs. The secondary bronchi form the tertiary
bronchi, which go to each lobule of the lung. The tertiary bronchi branch many times to
form the bronchioles.
The Lower Respiratory Tract:The Respiratory Tree The bronchioles branch to form the
terminal bronchioles, which become the respiratory bronchioles, from which the alveoli branch.
The epithelium from the trachea to the terminal bronchioles is ciliated to facilitate the removal of debris.
Cartilage helps to hold the tube system open (from the trachea to the bronchioles).
The Lower Respiratory Tract:The Respiratory Tree Smooth muscle controls the diameter f
the tubes (especially the bronchioles). The alveoli are sacs formed by simple
squamous epithelium, and they facilitate the diffusion of gases.
The Lower Respiratory Tract:The Lungs
The Lower Respiratory Tract:The Alveoli
Mechanics of Breathing
Mechanics of Breathing Ventilation is the movement of air into and
out of the lungs. Air moves from an area of higher pressure to an area of lower pressure.
Inspiration occurs when the diaphragm contracts and the external intercostal muscles lift the ribcage, thus increasing the volume of the thoracic cavity.
Expiration occurs when the diaphragm relaxes and the internal intercostal muscles depress the ribcage, thus decreasing the volume of the thoracic cavity.
Mechanics of Breathing
Mechanics of Breathing Lungs tend to collapse because of the
elastic recoil of the connective tissue, and surface tension of the fluid lining the alveoli.
The lungs normally do not collapse because surfactant reduces the surface tension of the fluid lining the alveoli, and the visceral pleura tends to adhere to the parietal pleura.
Pulmonary Volumes and Capacities There are four pulmonary volumes: tidal
volume, inspiratory reserve volume, expiratory reserve volume, and residual volume.
The tidal volume refers to the volume of air that goes into and out of the lungs during normal respiration (about 500 cc).
The inspiratory reserve volume is the amount of air that can be inspired forcefully after inspiration of the normal tidal volume (about 3000 cc).
Pulmonary Volumes and Capacities The expiratory reserve volume is the
additional amount of air that can be expired forcefully (about 1100 cc).
The residual volume is the volume of air left in the lungs after maximum expiration. This is also known as “dead space” (about 1200 cc).
Pulmonary Volumes and Capacities The pulmonary capacities refer to the
sum of two or more pulmonary volumes. The vital capacity is the sum of the IRV,
the TV and the ERV. It is the maximum volume of air that a person can expel from his respiratory tract after a maximum inspiration (about 4600 cc).
VC = IRV + TV + ERV
Pulmonary Volumes and Capacities The inspiratory capacity is the amount of
air that a person can inspire maximally after a normal expiration (about 3500 cc).
IC = TV + IRV The functional residual capacity is the
amount of air remaining in the lungs at the end of a normal expiration (about 2300 cc).
FRC = ERV + RV The total lung capacity is the sum of all the
lung volumes (about 5800 cc).
TV
MAXIMUM
EXPIRATION
RV
IRV
ERV
VC
MAXIMUM
INSPIRATION
RV
IC
FRC
TOTAL
LUNG
CAPACITY
Pulmonary Volumes and Capacities
Pulmonary Pressures Major factors in determining the extent of
lung expansion and compliance during the processes of inspiration and expiration: Alveolar pressure Intrapleural pressure Alveolar surfactant
During inspiration, the thoracic cage enlarges, enlarging both lungs and decreasing the pressures.
Pulmonary Pressures Boyle’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 Pressures Boyle’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 Pressures Intrapleural Pressures:
Intrapleural space is the space between the lungs and the outer walls of the thoracic cavity. The pressure here is ALWAYS a few mmHg less than in the alveoli for the following reasons:
Surface tension of the fluid inside the alveoli always makes the alveoli try to collapse.
Elastic fibers spread in all directions through the lung tissues and tend to contract the lungs.
These factors pull the lungs away from the outer walls of the pleural cavity, creating an average negative pressure of –5 mmHg.
Pulmonary Pressures Surfactant:
Surface active agent Detergent that greatly decreases the
surface tension of fluid lining the alveoli.
Essential Requirements for Ventilation Adequate atmospheric oxygen Clean air passages Adequate pulmonary compliance and
recoil Compliance is the expansibility or
stretchability of the lungs. Recoil is the ability to collapse away from
the chest wall due to (1) elastic fibers present in the lungs, and (2) surface tension of the fluid lining of the alveoli which accounts for 2/3 of the recoil phenomenon.
Gas Exchange The respiratory membranes are thin and
have a large surface area that facilitates gas exchange.
The components of the respiratory membrane include a film of water, the walls of the alveoli, and interstitial space, and the walls of the perialveolar capillary.
Gas Exchange The rate of diffusion depends on the
thickness of the respiratory membrane, the surface area of the membrane, the diffusion coefficient of the gas, and the partial pressure of gases in the alveoli and in the blood.
Transport of Oxygen and Carbon Dioxide 97% of oxygen combines loosely with
hemoglobin in the red blood cells and is carried into the tissues as oxyhemoglobin. The remaining oxygen is dissolved and transported in the fluid of plasma and cells.
The amount of oxygen that the blood will absorb before it is fully saturated is about 20 ml per 100 ml of blood (20 vol%).
Transport of Oxygen and Carbon Dioxide As the hemoglobin releases oxygen to
the tissues, it is referred to as reduced hemoglobin.
Normally, only about 25% of oxygen per ml of blood is diffused to the tissue (5 vol%). However, this rate of release can be increased to 75% during periods of stress or increased exercise.
Transport of Oxygen and Carbon Dioxide Factors that influence the rate of
oxygen transport from the lungs to the tissues: Cardiac output Erythrocyte count Exercise Hematocrit
Control of Respiration The respiratory center in the medulla
oblongata and pons stimulates the muscles of inspiration to contract. When stimulation of the muscles of inspiration stops, expiration occurs passively.
Control of Respiration Receptors present in the respiratory and
cardiovascular system, as well as in other parts of the body, receive changes in the internal milieu and send sensory signals to the respiratory center. Receptors are classified as: chemoreceptors, baroreceptors, proprioceptors, and stretch receptors.
Control of Respiration The Hering-Breuer reflex inhibits the
inspiratory center when the lungs are stretched during inspiration.
Carbon dioxide is the major chemical regulator of respiration.
It is possible to consciously control ventilation, but only up to a certain degree.
The Cough and Sneeze Reflexes
The Cough and Sneeze Reflexes Means for keeping the respiratory
passages clean by forcing air very rapidly outward using these two reflexes.
Mediated by respiratory muscles, voluntary and involuntary, with regulation by the central nervous system and sensory receptors lining the respiratory tract.
The Cough Reflex
Irritant touches the surface of the glottis, trachea or bronchus.
Sensory signals are transmitted to the medulla.
Motor signals are transmitted back to the respiratory system.
The Cough Reflex
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 Reflex
Irritant comes into contact with sensory receptors in the nose.
Sensory signals are received in the medulla.
Motor signals are generated and transmitted back.
The Sneeze Reflex
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.
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.
Symptoms of Pulmonary Disease Persistent cough
Always abnormal Chronic persistent cough may be caused by
cigarette smoking, asthma, bronchiectasis or COPD.
May also be caused by drugs, cardiac disease, occupational agents and psychogenic factors.
Complications include (1) worsening of bronchospasm, (2) vomiting, (3) rib fractures, (4) urinary incontinence, and (5) syncope.
Symptoms of Pulmonary Disease 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.
Symptoms of Pulmonary Disease 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.
Signs of Pulmonary Disease 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.
Signs of Pulmonary Disease 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.
Signs of Pulmonary Disease 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
Signs of Pulmonary Disease Physical chest deformities
The 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 volume
Signs of Pulmonary Disease Physical chest deformities
Symmetrically 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
Signs of Pulmonary Disease Physical chest deformities
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
Signs of Pulmonary Disease Pulsus paradoxicus
The 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
Signs of Pulmonary Disease Cyanosis
Bluish discoloration of skin or mucous membranes.
Caused by increased amounts (>5 g/dL) of unsaturated / reduced hemoglobin.
Presents as either central or peripheral cyanosis
Signs of Pulmonary Disease Digital clubbing
Anteroposterior 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
Signs of Pulmonary Disease Percussion sounds (resonance, dullness,
hyperresonance) Auscultatory sounds (vesicular,
bronchial, bronchovesicular) Adventitious sounds
Abnormal sounds on auscultation May be classified as continuous (wheezes,
rhonchi) or discontinuous (crackles, crepitations)
Signs of Pulmonary Disease 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.
Signs of Pulmonary Disease 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.
Signs of Pulmonary Disease Fremitus
Voice 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.
Signs of Pulmonary Disease Whispered pectoriloquy
Extreme 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.
Signs of Pulmonary Disease
TYPICAL CHEST EXAMINATION FINDINGS IN SELECTED CLINICAL CONDITIONS
CONDITION PERCUSSION
FREMITUS BREATH SOUNDS
VOICE TRANSMISSIO
N
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
Signs of Pulmonary Disease
TYPICAL CHEST EXAMINATION FINDINGS IN SELECTED CLINICAL CONDITIONS
CONDITION PERCUSSION FREMITUS BREATH SOUNDS
VOICE TRANSMISSIO
N
ADVENTITIOUS SOUNDS
Interstitial Lung Disease
Resonant Normal Vesicular Normal Crackles
Emphysema Hyperresonant
Decreased
Decreased
Decreased Absent or wheezing
Pneumothorax
Hyperresonant
Decreased
Decreased
Decreased Absent
Pleural effusion
Dull Decreased
Decreased
Decreased Absent or pleural
friction rub
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.
Routine Radiography Apicolordotic views visualize disease at
the lung apices better than the standard posteroanterior view.
Chest Radiography
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.
Computed Tomography
Computed Tomography
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.
Pulmonary Function Tests Indications:
Evaluation of the type and degree of pulmonary dysfunction (obstructive or restrictive)
Evaluation of dyspnea, cough and other symptoms
Early detection of lung dysfunction Surveillance in occupational settings Follow-up or response to therapy Preoperative evaluation Disability assessment
Pulmonary Function Tests Relative contraindications:
Severe acute asthma or respiratory distress Chest pain aggravated by testing Pneumothorax Brisk hemoptysis Active tuberculosis
Pulmonary Function Tests 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.
TV
MAXIMUM
EXPIRATION
RV
IRV
ERV
VC
MAXIMUM
INSPIRATION
RV
IC
FRC
TOTAL
LUNG
CAPACITY
Pulmonary Volumes and Capacities
Pulmonary Function Tests Ventilation-Perfusion Lung Scan (V/Q
scan) Measures the degree of ventilation of the
individual lung segments and the perfusion of respective segments to detect any shunting or mismatch.
Finds utility in settings where possible pulmonary embolism is suspected.
The Lower Respiratory Tract:The Lungs
Arterial Blood Gases Measure of acid and base balance in the
blood. Also check the saturation of blood with
oxygen.
Biologic Specimen Collection Sputum collection
Spontaneous expectoration or sputum induction
Percutaneous needle aspiration Usually carried out under CT or ultrasound
guidance. Potential risks include intrapulmonary
bleeding and creation of a pneumothorax.
Biologic Specimen Collection Thoracentesis
Sampling of pleural fluid or for palliation of dyspnea in patients with pleural effusion.
Analysis of the fluid for cellular composition and chemical constituents like glucose, protein and LDH.
Biologic Specimen Collection Bronchoscopy
Provides for direct visualization of the tracheobronchial tree.
Rigid bronchoscopy is performed in an operating room on a patient under general anesthesia.
Flexible bronchoscopy may be done under local anesthesia / sedation.
Diagnostic uses include histologic identification or neoplasms and identification of sources of hemoptysis.
Biologic Specimen Collection Bronchoscopy
Therapeutic indications are retrieval of foreign bodies and control of bleeding.
Bronchoalveolar lavage has been used for the recovery of organisms that are difficult to isolate in the usual sputum recovery methods.
Biologic Specimen Collection Video-Assisted Thoracic Surgery (VATS)
Operator can biopsy lesions of the pleura under direct vision for both diagnostic and therapeutic purposes.
Thoracotomy Frequently replaced by VATS. Provides the largest amount of biologic
specimen for histologic study.
Biologic Specimen Collection Mediastinoscopy and Mediastinotomy
Both performed under general anesthesia by a qualified surgeon.
Used for visualization and sampling of tissues in the mediastinum such as lymph nodes and neoplasms.
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.
Influenza: 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 headache Fever and chills Myalgia and malaise Cough, sneezing and sore throat
Influenza: Clinical Manifestations The major problem posed consists of its
complications: Primary influenza viral pneumonia Secondary bacterial pneumonia Mixed viral and bacterial pneumonia Extrapulmonary complications:
Reye’s syndrome Myositis, rhabdomyolysis and myoglobinuria Encephalitis, transverse myelitis Guillain-Barré syndrome
Influenza: 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)
Influenza: Treatment 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.
Viral Rhinitis 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.
Viral Rhinitis: Clinical Manifestations Incubation period of 1 to 2 days. Illness generally lasts 4 to 9 days and
resolves spontaneously. Symptoms:
Headache Nasal congestion Water rhinorrhea Sneezing Scratchy throat General malaise and occasionally fever
Viral Rhinitis: Clinical Manifestations Signs:
Reddened, edematous nasal mucosa Water 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.
Viral Rhinitis: Clinical Manifestations Complications:
Transient middle ear effusion Secondary 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.
Viral Rhinitis: 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).
Antipyretics Liberal fluid intake Ascorbic acid
Other Viral URTI:Coronavirus Account 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 Virus Belongs 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.
Other Viral URTI:Respiratory Syncytial Virus Clinical Manifestations:
Rhinorrhea Low-grade fever Mild systemic symptoms Cough and wheezing 25-40% 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 cough Acute febrile illness with coryza Barking cough and frank stridor in children
Other Viral URTI:Parainfluenza Virus 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.
Other Viral URTI:Adenovirus Clinical Manifestations:
Rhinitis Pharyngoconjunctival 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.
Other Viral URTI:Adenovirus 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.
Acute Bacterial Sinusitis Typical Pathogens:
Streptococcus pneumoniae Other streptococci Haemophilus influenzae Staphylococcus aureus Moraxella catarrhalis
Acute Bacterial Sinusitis Symptoms and Signs:
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.
Acute Bacterial Sinusitis Imaging:
Transillumination Caldwell view (frontal) Waters view (maxillary) Lateral view (sphenoid) Submentovertical view (ethmoid) CT scan for recurrent sinusitis MRI if malignancy in suspected
Acute Bacterial Sinusitis: Treatment Uncomplicated:
Outpatient management Oral decongestants and nasal decongestant
sprays Appropriate 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.
Acute Bacterial Sinusitis Complications:
Lower respiratory tract infections Osteomyelitis and mucocoele Intracranial complications Malignancy (?)
Allergic Rhinitis
Allergic Rhinitis “Hay fever” Symptoms mimic that of viral rhinitis but
more persistent and show seasonal variation.
Symptoms: Watery rhinorrhea Eye irritation, pruritus, erythema and tearing
Signs: Pale or violaceous turbinates Occasional polyposis
Allergic Rhinitis: Treatment Symptomatic in most cases. Oral decongestants Antihistamines Nasal corticosteroid sprays Maintaining an allergen-free
environment Air purifiers and dust filters Desensitization
Epistaxis Bleeding from Kiesselbach’s plexus Predisposing factors:
Nasal trauma (nose picking, foreign bodies, forceful nose blowing)
Rhinitis Drying of the nasal mucosa from low
humidity Nasal septal deviation Alcohol use Antiplatelet medications Bleeding diathesis
Epistaxis 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 sprays Cautery Treatment of other possible underlying
causes of bleeding
Acute Laryngitis Most common cause of vocal hoarseness. May persist for a week or so after
symptoms of upper airway infection have cleared.
Etiologies: Viral Bacterial (Moraxella catarrhalis, Haemophilus
influenzae) Treatment:
Avoid vigorous use of voice Erythromycin and other macrolides
Diseases of the Respiratory System
Diseases of the Airways
Diseases of the Respiratory System
Obstructive Airway Diseases
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.
Asthma Airway narrowing results from:
Smooth muscle spasm Airway edema and inflammation Mucus plugging
Variants: Exercise-induced asthma Triad asthma Cardiac asthma Asthmatic bronchitis Drug-induced asthma
Asthma
Asthma Pathogenesis:
Common denominator is nonspecific hyperirritability of the tracheobronchial tree.
Airway reactivity increased by: Allergenic Pharmacologic Environmental, occupational Infectious Emotional Activity-related
Asthma Symptoms and Signs:
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
Asthma Laboratory Findings:
Increased WBC count with eosinophilia Viscid sputum on gross examination Curschmann’s spirals on microscopic
examination of sputum Charcot-Leyden crystals Obstructive pattern on the pulmonary
function tests Diminished peak expiratory flow rate (normal:
450-650 L/min in men; 350-500 L/min in women)
Respiratory alkalosis and mild hypoxemia in ABGs.
Asthma
Asthma
Asthma
Asthma
Asthma Complications:
Exhaustion Dehydration Airway infection Cor pulmonale Tussive syncope Pneumothorax (rare)
Asthma Prevention:
Comprehensive patient education Pharmacologic intervention Environment control Early treatment of chest infections Recognition and effective management of
nasal and paranasal disorders Discontinuance of cigarette smoking Pneumococcal and yearly influenza
immunization for patients with moderate to severe asthma
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.
Asthma: Classifications 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.
Asthma: Classifications Severe asthma:
Continuous symptoms Frequent exacerbations Limitations of physical activities Frequent nocturnal symptoms Requirement for frequent emergency care PEFR 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)
Asthma: Treatment Mild ambulatory asthma:
Short-acting inhaled β2-agonist drug Moderate ambulatory asthma:
Daily maintenance therapy with inhaled corticosteroids
Cromolyn or nedocromil Short-acting inhaled β2-agonist drugs for
breakthrough wheezing Oral theophylline
Asthma: Treatment
Asthma: Treatment Severe ambulatory asthma:
Daily maintenance therapy with inhaled corticosteroids
Daily oral sustained-release theophylline or oral β2-agonist drugs
Long-acting inhaled β2-agonist drug (salmeterol)
Inhaled anti-cholinergic drug (ipratropium bromide)
Short-acting inhaled β2-agonist drug for breakthrough wheezing
Oral steroids
Asthma: Treatment Status asthmaticus:
Supplemental oxygen, 1-3 L/min Monitoring with oximetry Inhaled β2-agonist agents Intravenous aminophylline Subcutaneous terbutaline Intravenous corticosteroids Inhaled corticosteroids Oral corticosteroids Supportive: hydration, physical therapy, MV
Asthma: 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.
Chronic Obstructive Pulmonary Disease (COPD)
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”
Chronic Obstructive Pulmonary Disease (COPD)
EMPHYSEMA VS CHRONIC BRONCHITIS
EMPHYSEMA CHRONIC BRONCHITIS
PHYSICAL EXAMINATION
Body habitus Thin, wasted Stocky, obese
Central cyanosis Absent Present
Plethora Absent Present
Accessory respiratory muscles
Hypertrophied Unremarkable
Anteroposterior chest diameter
Increased Normal
Percussion note Hyperresonant Normal
Auscultation Diminished breath sounds
Wheezes, rhonchi
Chronic Obstructive Pulmonary Disease (COPD)
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
Chronic Obstructive Pulmonary Disease (COPD)
EMPHYSEMA VS CHRONIC BRONCHITIS
EMPHYSEMA CHRONIC BRONCHITIS
LABORATORY INDICES
Hematocrit Normal Increased
ECG Normal RAD, RVH, P pulmonale
Hypoxemia Absent, mild Moderate, severe
Hypercapnia Absent Moderate, severe
Respiratory acidosis
Absent Present
Total lung capacity Increased Normal
Static lung compliance
Increased Normal
Diffusing capacity Decreased Normal
Chronic Obstructive Pulmonary Disease (COPD) Causes:
Cigarette smoking Air pollution Airway infection Familial factors Allergies
Chronic Obstructive Pulmonary Disease (COPD) Symptoms and Signs:
5th or 6th decade of life Excessive cough and sputum production Shortness of breath that have often been
present for 10 years or more Laboratory findings:
Secondary polycythemia Presence of microorganisms in the sputum Spirometry shows obstructive pattern Hyperinflation on radiographs
Chronic Obstructive Pulmonary Disease (COPD) Complications:
Pneumonia and acute bronchitis Pulmonary embolization Left ventricular heart failure Pulmonary hypertension Chronic respiratory failure Spontaneous pneumothorax
Chronic Obstructive Pulmonary Disease (COPD) Prevention:
Smoking cessation Early treatment of airway infections Vaccination against pneumococcal
pneumonia and influenza.
Chronic Obstructive Pulmonary Disease (COPD) Treatment:
Discontinuance of cigarette smoking Patient education Relief of bronchospasm
Ipratropium bromide Maintenance therapy with oral theophylline Oral corticosteroids
Aerosol therapy Chest physiotherapy Treatment of complications Home 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
Bronchiectasis 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.
Bronchiectasis Treatment:
Antibiotics Daily chest physiotherapy with postural
drainage and chest percussion Inhaled bronchodilators Surgical resection Diagnostic and therapeutic bronchoscopy
Complications: Cor pulmonale Amyloidosis Visceral 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
Community-Acquired Pneumonia: Pathophysiology
Community-Acquired Pneumonia: Pathophysiology
Community-Acquired Pneumonia Laboratory findings:
Leukocytosis Patchy 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
Community-Acquired Pneumonia
Community-Acquired Pneumonia:
Community-Acquired Pneumonia: Management Guidelines 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 vaccine Influenza vaccine
Community-Acquired Pneumonia: Management 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
Community-Acquired Pneumonia: Management 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
Community-Acquired Pneumonia: Management Treatment:
Should be directed towards the elimination of the suspected causative organism.
Respiratory support Isolation 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.
Hospital-Acquired Pneumonia Most common pathogens:
Pseudomonas aeruginosa Staphylococcus aureus Enterobacter sp. Klebsiella pneumoniae Escherichia 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 sweats
Cough Patients often appear chronically ill. Post-tussive apical rales.
Pulmonary Tuberculosis 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).
Pulmonary Tuberculosis Pathogenesis (cont’d):
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.
Pulmonary Tuberculosis Laboratory findings:
Recovery of Mycobacterium tuberculosis from cultures, or identification of organisms by DNA probe
Acid-fast bacilli in the sputum Serologic diagnosis by ELISA Apical infiltrates on chest radiographs Ghon and Ranke signs Tuberculin skin test
Pulmonary Tuberculosis
Pulmonary Tuberculosis
Pulmonary Tuberculosis
Pulmonary Tuberculosis
Pulmonary Tuberculosis
Pulmonary Tuberculosis
Pulmonary Tuberculosis
Pulmonary Tuberculosis
Pulmonary Tuberculosis 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.
Pulmonary Tuberculosis Sputum collection (cont’d):
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.
Pulmonary Tuberculosis Sputum collection (cont’d):
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.
Pulmonary Tuberculosis 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.
Pulmonary Tuberculosis PTB Classifications:
Class I: exposure, no symptoms, no radiographic evidence
Class II: exposure, (+) symptoms, no radiographic evidence
Class III: active PTB; exposure, (+) symptoms, (+) radiographic evidence
Class IV: treated PTB Class V: indeterminate
Pulmonary Tuberculosis: 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.
Pulmonary Tuberculosis: Treatment 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 + Ethambutol
Maintenance 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.
Pulmonary Tuberculosis: Treatment Areas with high resistance rates:
National Capital Region, including Laguna Cebu Davao Zamboanga Cavite Pampanga
Areas with low resistance rates: Palawan Mountain Province and Benguet
Pulmonary Tuberculosis: Treatment 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).
Pulmonary Tuberculosis: Treatment 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
Pulmonary Tuberculosis: Treatment 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 smoking Ionizing radiation Asbestos Heavy metals Industrial agents Lung scars Air pollution Genetic predisposition
Bronchogenic Carcinoma 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.
Bronchogenic Carcinoma Initial Symptoms:
Cough Weight loss Dyspnea Chest pain Hemoptysis Change in the patterns of the symptoms
Bronchogenic Carcinoma Physical findings vary and may be
totally absent: Superior vena cava syndrome Horner’s syndrome Pancoast’s syndrome Recurrent laryngeal nerve palsy with
diaphragmatic hemiparesis Paraneoplastic syndromes
Bronchogenic CarcinomaPARANEOPLASTIC 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
Bronchogenic CarcinomaPARANEOPLASTIC 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
Bronchogenic Carcinoma 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:
Surgery Chemotherapy Radiotherapy Combination therapy Immunomodulation
Bronchogenic Carcinoma 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.
Pulmonary Thromboembolism Physiologic risk factors:
Venous stasis Venous endothelial injury Hypercoagulability
Oral contraceptives Cancer Protein C or S deficiency Antithrombin III deficiency
Pulmonary Thromboembolism Clinical risk factors:
Prolonged bed rest or inactivity Surgery Childbirth Advanced age Stroke Myocardial infarction Congestive heart failure Obesity Fractures of the hip or femur
Pulmonary Thromboembolism Symptoms:
Pleuritic chest pain (74%) Non-pleuritic chest pain (14%) Dyspnea (84%) Apprehension (59%) Cough (53%) Hemoptysis (30%) Sweats (27%) Syncope (13%)
Pulmonary Thromboembolism 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%)
Pulmonary Thromboembolism 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
Pulmonary Thromboembolism Prevention:
Critically important Identification of those at risk Prophylaxis
Treatment: Anticoagulation Thrombolytic therapy Inferior vena cava filter
Pulmonary Thromboembolism 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.
Inhalation of Air Pollutants Prognosis:
Depends on the severity and type of exposure.
Also depends on the patient’s preexisting pulmonary status.
Inhalation of Air Pollutants
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
Inhalation of Air Pollutants
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.
Pulmonary Aspiration Syndromes Retention of an aspirated foreign body Chronic aspiration of gastric contents Mendelson’s syndrome
Disorders of Ventilation Obesity-hypoventilation syndrome
(Pickwickian syndrome) Sleep-related breathing disorders Obstructive sleep apnea Hyperventilation syndrome
Acute Respiratory Failure Clinical Findings:
Signs and symptoms of the underlying disease
Hypoxemia and hypercapnia Dyspnea is the chief symptom. Cyanosis Restlessness, confusion, anxiety, delirium Tachypnea Tachycardia, hypertension, cardiac
arrhythmias Tremors
Acute Respiratory Failure: 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
Acute Respiratory Failure: Treatment Ventilatory respiratory support
Mechanical ventilation Apnea Acute hypercapnia Severe hypoxemia Progressive patient fatigue
Acute Respiratory Failure: Treatment General supportive care
Nutritional support Maintenance of fluid and electrolyte balance Psychological and emotional support Skin care to avoid decubitus ulcers Meticulous avoidance of nosocomial
infections Prevention 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
Pleural Effusion 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
Pleural Effusion: Approach to Management
PLEURAL 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
Pleural Effusion: Approach to Management
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
Pleural Effusion: Approach to Management
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
Pleural Effusion Treatment:
Treatment of the underlying condition Removal if the effusion is large (therapeutic
thoracentesis or tube thoracostomy) Pleurodesis
Pneumothorax Types:
Spontaneous Traumatic
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.
Pneumothorax Treatment:
Depends on the severity of the condition. Supportive and oxygen supplementation if
needed. Tube thoracostomy and pleurodesis.