respiratory

“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


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


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

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

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 Airways


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 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”




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




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




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


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 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 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.


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


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


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

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.

respiratory

Documents

frc rv rv

acute bacterial sinusitis

respiratory tract irritation

upper respiratory tract

bronchogenic carcinomaparaneoplastic syndromes

lower respiratory tract

expiratory reserve volume

newly diagnosed ptb