Roses Are Red, Violets Are Blue, Without Your Lungs Your Blood Would Be, Too.

Roses are red, Violets are blue, Without your lungs Your blood would be, too.
David D. Ralph, MD
New England Journal of Medicine
MEDICAL-SURGICAL 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.
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.
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.
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 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 superior part of the nasal cavity contains the sensory cells for the sense of smell. A vast network of capillaries, called Kiesselbachs plexus, line the mucosa of the nasal cavity.
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 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 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.
It is lined by pseudostratified ciliated columnar epithelium which aids in the filtering of inhaled air.
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 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 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).
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
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.
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).
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).
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
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).

MAXIMUM INSPIRATION
IRV IC VC TV TOTAL LUNG CAPACITY
ERV
MAXIMUM EXPIRATION
FRC RV RV
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
Boyles 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
Boyles 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%).
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.
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.
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.
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

Motor signals are transmitted back to the respiratory system.
Respiratory muscles contract rapidly generating high pressures in the lungs while the vocal cords remain tightly closed.
Vocal cords open suddenly, allowing pressurized air in the lungs to flow out in a blast.
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

Motor signals are generated and transmitted back.
Respiratory muscles contract rapidly generating high pressures in the lungs while the vocal cords remain tightly closed.
Vocal cords open suddenly, allowing pressurized air in the lungs to flow out in a blast through the nose and mouth.
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.

Dyspnea on recumbency. Dyspnea on the upright position relieved by recumbency.
Orthopnea
Platypnea
Persistent cough

Always abnormal Chronic persistent cough may be caused by cigarette smoking, asthma, bronchiectasis or COPD. May also be caused by drugs, cardiac disease, occupational agents and psychogenic factors. Complications include (1) worsening of bronchospasm, (2) vomiting, (3) rib fractures, (4) urinary incontinence, and (5) syncope.
Stridor

Crowing sound during breathing. Caused by turbulent airflow through a narrowed upper airway. Inspiratory stridor implies extratracheal variable airway obstruction. Expiratory stridor implies intratracheal variable airway obstruction. Stertorous breathing is an inspiratory sound due to vibration in the pharynx during sleep.
Wheezing
Continuous musical or whistling noises caused by turbulent airflow through narrowed intrathoracic airways. Most, but not all, are due to asthma. 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.
Hemoptysis

Signs of Pulmonary Disease
Tachypnea

Rapid, shallow breathing. Arbitrarily defined as a respiratory rate in excess of 18/min. Slow breathing. Rapid, deep breathing. Increase in the amount of air entering the alveoli.
Bradypnea
Hyperpnea
Hyperventilation
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. 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.
Cheyne-Stokes respiration

Biot breathing

Uncommon variant of Cheyne-Stokes respiration. Periods of apnea alternate irregularly with series of breaths of equal depth that terminate abruptly. Most often seen in meningitis.
Singultus
Sudden, involuntary diaphragmatic contraction producing an inspiration interrupted by glottal closure to emit a characteristic sharp sound. Causes:

Reflex stimulation without organic disease Diseases of the central nervous system Mediastinal disorders Pleural irritation Abdominal disorders Diaphragmatic stimulation
Physical chest 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 Unilateral airway obstruction Pleural or pulmonary fibrosis Splinting due to chest pain Pleural effusion Pneumothorax
Asymmetric chest expansion during inspiration:

Expansion on the chest, collapse of the abdomen on inspiration:
Weakness or paralysis of the diaphragm Airway obstruction Intercostal muscle paralysis Flail deformity of the chest
Chest collapse, rise of the abdomen on inspiration:

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
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
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
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)
Wheezes
High-pitched sounds which results from bronchospasm, bronchial or bronchiolar mucosal edema, or airway obstruction by mucus, tumors, or foreign bodies. Low-pitched sounds caused by sputum in large airways and frequently clear after coughing.
Rhonchi
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.
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. Increased intensity and clarity of the spoken word during auscultation. Heard over areas of consolidation or lung compression.
Bronchophony
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.

TYPICAL CHEST EXAMINATION FINDINGS IN SELECTED CLINICAL CONDITIONS CONDITION Normal Consolidation or Atelectasis (with patent airway) PERCUSSION Resonant Dull FREMITUS Normal Increased BREATH SOUNDS Vesicular Bronchial VOICE TRANSMISSION Normal Bronchophony, whispered pectoriloquy, egophony ADVENTITIOUS SOUNDS Absent Crackles
Consolidation or Atelectasis (with blocked airway)

Bronchial Asthma
Dull
Decreased
Decreased
Decreased
Absent
Resonant
Normal
Vesicular
Normal
Wheezing

TYPICAL CHEST EXAMINATION FINDINGS IN SELECTED CLINICAL CONDITIONS CONDITION Interstitial Lung Disease Emphysema Pneumothorax Pleural effusion PERCUSSION Resonant Hyperresonant Hyperresonant Dull FREMITUS Normal Decreased Decreased Decreased BREATH SOUNDS Vesicular Decreased Decreased Decreased VOICE TRANSMISSION Normal Decreased Decreased Decreased ADVENTITIOUS SOUNDS Crackles Absent or wheezing Absent 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.
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
Relative contraindications:

Severe acute asthma or respiratory distress Chest pain aggravated by testing Pneumothorax Brisk hemoptysis Active tuberculosis
Spirometry
Allows for the determination of the presence and severity of obstructive and restrictive pulmonary dysfunction. The hallmark of obstructive pulmonary dysfunction is reduction of airflow rates. Restrictive pulmonary dysfunction is characterized by reduction in pulmonary volumes.

MAXIMUM INSPIRATION
IRV IC VC TV TOTAL LUNG CAPACITY
ERV
MAXIMUM EXPIRATION
FRC RV RV
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 Usually carried out under CT or ultrasound guidance. Potential risks include intrapulmonary bleeding and creation of a pneumothorax.
Percutaneous needle aspiration
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.
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.
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.
Video-Assisted Thoracic Surgery (VATS)
Operator can biopsy lesions of the pleura under direct vision for both diagnostic and therapeutic purposes. Frequently replaced by VATS. Provides the largest amount of biologic specimen for histologic study.
Thoracotomy

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 patients 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:

Reyes syndrome Myositis, rhabdomyolysis and myoglobinuria Encephalitis, transverse myelitis Guillain-Barr syndrome
Influenza: Treatment
Treatment for uncomplicated influenza is symptomatic
Salicylates should be avoided in children because of its association with Reyes 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
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.
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.
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.
Diagnosis and Treatment:

Diagnosis is established by isolation of the virus. No specific antiviral therapy is available. A live oral vaccine is available and used widely to prevent outbreaks among military recruits.
Acute Bacterial Sinusitis
Symptoms of rhinitis plus clinical signs and symptoms that indicate involvement of the affected sinus or sinuses such as pain and tenderness over the involved sinus. Occurs when an undrained collection of pus accumulates in a sinus.
Typical Pathogens:

Streptococcus pneumoniae
Other streptococci
Haemophilus influenzae Staphylococcus aureus Moraxella catarrhalis
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.
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.
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 Kiesselbachs 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 patients 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 Exercise-induced asthma Triad asthma Cardiac asthma Asthmatic bronchitis Drug-induced asthma
Variants:

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 Curschmanns 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.
Moderate asthma:

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

Continuous 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 2-agonist drug Daily maintenance therapy with inhaled corticosteroids Cromolyn or nedocromil Short-acting inhaled 2-agonist drugs for breakthrough wheezing Oral theophylline
Moderate ambulatory asthma:
Asthma: Treatment
Asthma: Treatment
Severe ambulatory asthma:
Daily maintenance therapy with inhaled corticosteroids Daily oral sustained-release theophylline or oral 2-agonist drugs Long-acting inhaled 2-agonist drug (salmeterol) Inhaled anti-cholinergic drug (ipratropium bromide) Short-acting inhaled 2-agonist drug for breakthrough wheezing Oral steroids
Asthma: Treatment
Status asthmaticus:

Supplemental oxygen, 1-3 L/min Monitoring with oximetry Inhaled 2-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.
Abnormal and permanent enlargement of air spaces distal to the terminal bronchiole, with destruction of their walls, and without obvious fibrosis.
Emphysema

EMPHYSEMA VS CHRONIC BRONCHITIS EMPHYSEMA HISTORY Onset of symptoms Dyspnea Cough Sputum production Sputum appearance Other features After age 50 Progressive, constant, severe Absent or mild Absent or mild Clear, mucoid Weight loss pink puffer CHRONIC BRONCHITIS After age 35 Intermittent, mild to moderate Persistent, severe Copious Mucopurulent or purulent Airway infections, right heart failure, obesity blue bloater

EMPHYSEMA VS CHRONIC BRONCHITIS EMPHYSEMA PHYSICAL EXAMINATION Body habitus Central cyanosis Plethora Accessory respiratory muscles Anteroposterior chest diameter Percussion note Auscultation Thin, wasted Absent Absent Hypertrophied Increased Hyperresonant Diminished breath sounds CHRONIC BRONCHITIS Stocky, obese Present Present Unremarkable Normal Normal Wheezes, rhonchi

EMPHYSEMA VS CHRONIC BRONCHITIS EMPHYSEMA CHEST X-RAY Bullae, blebs Overall appearance Hyperinflation Heart size Hemidiaphragms Present Decreased markings in the periphery Present Normal or small, vertical Low, flat CHRONIC BRONCHITIS Absent Dirty lungs Absent Large, horizontal Normal, rounded

EMPHYSEMA VS CHRONIC BRONCHITIS EMPHYSEMA LABORATORY INDICES Hematocrit ECG Hypoxemia Hypercapnia Respiratory acidosis Total lung capacity Normal Normal Absent, mild Absent Absent Increased CHRONIC BRONCHITIS Increased RAD, RVH, P pulmonale Moderate, severe Moderate, severe Present Normal
Static lung compliance

Diffusing capacity
Increased
Decreased
Normal
Normal
Causes:

Cigarette smoking Air pollution Airway infection Familial factors Allergies
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 Secondary polycythemia Presence of microorganisms in the sputum Spirometry shows obstructive pattern Hyperinflation on radiographs
Laboratory findings:

Complications:

Pneumonia and acute bronchitis Pulmonary embolization Left ventricular heart failure Pulmonary hypertension Chronic respiratory failure Spontaneous pneumothorax
Prevention:

Smoking cessation Early treatment of airway infections Vaccination against pneumococcal pneumonia and influenza.
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. 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: Pathophysiology

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: 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 Pneumococcal vaccine Influenza vaccine
Prevention:

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
Out-patient, with co-morbidity, age > 60 years old

Streptococcus pneumoniae
Respiratory viruses
Haemophilus influenzae Moraxella catarrhalis Streptococcus pneumoniae Haemophilus influenzae Legionella Staphylococcus aureus Chlamydia pneumoniae
Hospitalized patients with CAP

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

Pseudomonas aeruginosa Staphylococcus aureus Enterobacter sp. Klebsiella pneumoniae Escherichia coli
Empiric therapy must be started as soon as pneumonia is suspected. Respiratory support
Treatment:
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.
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 tissuedamaging 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).
Pathogenesis (contd):
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.
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
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.
Sputum collection (contd):

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.
Sputum collection (contd):
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 smearnegative or unable to expectorate sputum spontaneously.
Sputum TB culture and sensitivity tests:
Smear (-) patients with a strong clinical possibility of PTB and suggestive chest x-rays. Smear (+) or (-) patients suspected of multi-drug resistant PTB. Smear (+) patients demonstrating the rise fall phenomenon. All cases of relapse. All cases of re-treatment. All cases of treatment failure.
PTB Classifications:
Class I: exposure, no symptoms, no radiographic 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.
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 Next 3 months: Isoniazid and Rifampicin Check clinical profile. May discontinue after a total of 9 months, or may continue as clinical evidence dictates.
Maintenance Phase: 3/6HR

Areas with high resistance rates:

National Capital Region, including Laguna Cebu Davao Zamboanga Cavite Pampanga Palawan Mountain Province and Benguet
Areas with low resistance rates:

Empiric therapy for MDR-TB suspect:

Use of at least some second-line drugs. Prescribe drugs which the patient has not previously taken. The initial regimens should consist of at least three drugs, preferably four or five, to which the bacilli are likely to be fully sensitive (injectable aminoglycoside and pyrazinamide, even if previously used, because resistance is usually unlikely).
Hospitalization is not necessary in most patients, but should be considered if the patient is incapable of self-care. Preventive therapy:
Should be given if the patient is under 35 years of age with a positive tuberculin test (>10 mm) in the following conditions:
Foreign-born persons from countries with high prevalence of TB. Medically underserved, low-income groups Residents of long-term care facilities
Preventive therapy:

Isoniazid preventive therapy for 6 to 12 months. Vaccine:

BCG should be given to tuberculin-negative persons. Children who are repeatedly exposed to individuals with untreated or ineffectively treated TB also benefit from BCG vaccination.

Bronchogenic Carcinoma
Suspected etiologies:

Cigarette smoking Ionizing radiation Asbestos Heavy metals Industrial agents Lung scars Air pollution Genetic predisposition
Squamous cell carcinoma and adenocarcinoma are the most common types (30 to 35% of primary tumors each). Small cell carcinoma and large cell carcinoma account for about 20 to 25% and 15% of cases, respectively. 10 to 25% of patients are asymptomatic, especially during the early course of the disease.
Initial Symptoms:

Cough Weight loss Dyspnea Chest pain Hemoptysis Change in the patterns of the symptoms
Physical findings vary and may be totally absent:

Superior vena cava syndrome Horners syndrome Pancoasts syndrome Recurrent laryngeal nerve palsy with diaphragmatic hemiparesis Paraneoplastic syndromes
PARANEOPLASTIC SYNDROMES IN LUNG CANCER CLASSIFICATION ENDOCRINE AND METABOLIC SIADH Hypercalcemia Gynecomastia CONNECTIVE TISSUE AND OSSEOUS NEUROMUSCULAR Clubbing and hypertrophic pulmonary osteodystrophy Peripheral neuropathy Subacute cerebellar degeneration Myasthenia (Eaton-Lambert syndrome) Dermatomyositis SYNDROME Cushings syndrome COMMON HISTOLOGIC TYPE Small cell Small cell Squamous cell Large cell Squamous cell, large cell and adenocarcinoma Small cell Small cell Small cell All
PARANEOPLASTIC SYNDROMES IN LUNG CANCER CLASSIFICATION CARDIOVASCULAR SYNDROME Thrombophlebitis Nonbacterial verrucous (marantic) endocarditis HEMATOLOGIC Anemia Disseminated intravascular coagulation Eosinophilia Thrombocytosis CUTANEOUS Acanthosis nigricans Erythema gyratum repens COMMON HISTOLOGIC TYPE Adenocarcinoma Adenocarcinoma All All All All All All
Cytologic examination of sputum permits definitive diagnosis of lung cancer in 40 to 60% of cases. CT scan and other imaging techniques. Surgery Chemotherapy Radiotherapy Combination therapy Immunomodulation
Treatment:

Prognosis:

Over-all five-year survival rate is 10 to 15%. Determinants of survival:

Stage of disease at time of presentation Patients 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.
Physiologic risk factors:

Venous stasis Venous endothelial injury Hypercoagulability
Oral contraceptives Cancer Protein C or S deficiency Antithrombin III deficiency
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
Symptoms:

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

Tachypnea (92%) Crackles (58%) Accentuated split second heart sound (53%) Tachycardia (44%) Fever > 37.8C (43%) Phlebitis (32%) Diaphoresis (36%) Edema (24%) Murmur (23%) Cyanosis (19%)
Results of routine laboratory tests are not helpful in diagnosing pulmonary thromboembolism. Imaging and special examinations:

Chest radiography Lung scanning Venous thrombosis studies Pulmonary angiography
Prevention:

Critically important Identification of those at risk Prophylaxis Anticoagulation Thrombolytic therapy Inferior vena cava filter
Treatment:

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. 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.
Treatment:
Prognosis:

Depends on the severity and type of exposure. Also depends on the patients preexisting pulmonary status.

MAJOR AIR POLLUTANTS, SOURCES AND ADVERSE EFFECTS NOXIOUS AGENT OXIDES OF NITROGEN SOURCES Automobile exhaust; gas stoves and heaters; wood-burning stoves; kerosene space heaters Automobile exhaust, cigarette smoke Automobile exhaust, high altitude aircraft cabins ADVERSE EFFECTS Respiratory tract irritation, bronchial hyperreactivity, impaired lung defense, bronchiolitis obliterans Lung cancer Cough, substernal discomfort, bronchoconstriction, decreased exercise performance, respiratory tract irritation
HYDROCARBONS OZONE

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

Caf 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 Mendelsons 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
Ventilatory respiratory support
Mechanical ventilation

Apnea Acute hypercapnia Severe hypoxemia Progressive patient fatigue
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. Very low protein content Often seen in non-inflammatory states
Transudative effusion

Pleural Effusion: Approach to Management

PLEURAL EFFUSION
Perform diagnostic thoracentesis Measure pleural fluid protein and LDH
Any of the following met? PF/serum protein > 0.5 PF/serum LDH > 0.6 PF LDH > 2/3 upper normal serum limit
Yes
Further diagnostic procedures
No
EXUDATE
Treat CHF, cirrhosis, nephrosis
TRANSUDATE

Further diagnostic procedures
EXUDATE
Measure PF glucose, amylase Obtain PF cytology Obtain differential cell count Culture, stain PF
Amylase elevated Consider: esophageal rupture, Pancreatic pleural effusion Malignancy
Glucose < 60 mg/dL Consider: Malignancy Bacterial infections Rheumatoid pleuritis
NO DIAGNOSIS

NO DIAGNOSIS
Negative Needle biopsy of pleura Negative Consider pulmonary embolus (lung scan or pulmonary arteriogram) Positive: Treat for TB or CA Positive: Treat for TB Positive: Treat for PE
Negative
PPD
No: Consider Thoracoscopy or Open pleural biopsy
SYMPTOMS IMPROVING
Yes Observe
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.

Roses Are Red, Violets Are Blue, Without Your Lungs Your Blood Would Be, Too.

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Roses Are Red, Violets Are Blue, Without Your Lungs Your Blood Would Be, Too.

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Roses are red, Violets are blue, Without your lungs Your blood would be, too.

The Respiratory System

The Respiratory Process

The Respiratory Process

The Respiratory Process

The Respiratory Process

The Upper Respiratory Tract: The Nose

The Upper Respiratory Tract: The Nose

The Upper Respiratory Tract: The Nose

The Upper Respiratory Tract: The Nose

The Upper Respiratory Tract: The Pharynx

The Upper Respiratory Tract: The Pharynx

The Upper Respiratory Tract: The Larynx

The Upper Respiratory Tract: The Larynx

The Upper Respiratory Tract: The Larynx

The Upper Respiratory Tract: The Trachea

The Upper Respiratory Tract: The Trachea

The Upper Respiratory Tract: The Trachea

The Lower Respiratory Tract: The Respiratory Tree

The Lower Respiratory Tract: The Respiratory Tree

The Lower Respiratory Tract: The Respiratory Tree

The Lower Respiratory Tract: The Respiratory Tree

The Lower Respiratory Tract: The Lungs

The Lower Respiratory Tract: The Alveoli

Pulmonary Volumes and Capacities

Pulmonary Volumes and Capacities

Pulmonary Volumes and Capacities

Pulmonary Volumes and Capacities

Pulmonary Volumes and Capacities

IRV IC VC TV TOTAL LUNG CAPACITY

Alveolar pressure Intrapleural pressure Alveolar surfactant

Essential Requirements for Ventilation

Transport of Oxygen and Carbon Dioxide

Transport of Oxygen and Carbon Dioxide

As the hemoglobin releases oxygen to the tissues, it is referred to as reduced

Transport of Oxygen and Carbon Dioxide

Cardiac output Erythrocyte count Exercise Hematocrit

The Cough and Sneeze Reflexes

The Cough and Sneeze Reflexes

The Cough Reflex

Sensory signals are transmitted to the medulla.

Motor signals are transmitted back to the respiratory system.

The Cough Reflex

The Sneeze Reflex

Sensory signals are received in the medulla.

Motor signals are generated and transmitted back.

The Sneeze Reflex

Diagnosis of Pulmonary Function

Symptoms of Pulmonary Disease

Paroxysmal nocturnal dyspnea

Inappropriate breathlessness at night.

Symptoms of Pulmonary Disease

Symptoms of Pulmonary Disease

Symptoms of Pulmonary Disease

Signs of Pulmonary Disease

Signs of Pulmonary Disease

Kussmaul respiration (air hunger)

Signs of Pulmonary Disease

Signs of Pulmonary Disease

Signs of Pulmonary Disease

Physical chest deformities

Signs of Pulmonary Disease