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Terms in this set (23)

Dyspnea is what the individual says it is and is often described as "a breathlessness, air hunger, shortness of air/breath, and labored" Assessment findings often include: flaring nostrils, use of accessory muscles, and/or retraction of intercostal spaces. Orthopnea is a term that you may rember from cardiac content....orthopnea refers to dyspnea when lying flat (gravity puts pressure on the diaphragm). A form of severe orthopnea, called paroxysmal nocturnal dyspnea (PND), causes individuals to wake at night "gasping for air." Sitting/standing relieves the dyspnea.

Cough=protective reflex to fight the irritation of foreign bodies within the airway. Those who are not able to cough effectively are at greater risk for developing respiratory complications such pneumonia.

An acute cough usually lasts for 2-3 weeks and is usually result of a respiratory infection (laryngitis, pneumonia)

Long-term coughs (chronic coughs) involve a cough lasting longer than 3 weeks (sometimes 7-8 weeks depending on infection). Non-smoking related causes include postnasal drainage syndrome and asthma and smoking-related causes include chronic bronchitis and lung cancer.
When working with individuals that have a cough, something to assess is whether or not the cough is productive. If sputum is present, we want the patient to describe it (what it looks like). Earth-tone colors such as yellow or green may be a sign of infection. Also, if the sputum is thick, this could potentially block airway, so medication may be warranted. Bloody sputum/secretions is termed hemoptysis. Hemoptysis as a result of a cough is usually bright, red in color and indicates either an infection or damage within the lungs as a result of inflammation. Lung CA and PE are other causes (bloody sputum).
Hypoventilation involves inadequate alveolar ventilation and occurs when tidal volume and respiratory rate are reduced. Causes include altered pulmonary and/or neurologic function (e.g., brain stem—breathing center). Hypoventilation creates an environment in which CO2 within arterial blood (PaCO2) increases (AKA: hypercapnia). This type of environment results in respiratory acidosis.

Hyperventilation occurs when alveolar ventilation exceeds metabolic demands. The lungs remove CO2 so fast that it results in decreased levels of PaCO2 (hypocapnia). This type of environment results in respiratory alkalosis and interferes with tissue function. Causes include anxiety, acute head injury, and pain.

As you may recall, cyanosis (depicted on slide) is a bluish discoloration of the skin that results from increased amnts of desaturated or reduced hemoglobin within the blood. Cyanosis results with severe hypoxemia, so it manifests late in the game in relation to underlying complications. Other conditions, such as anemia and carbon monoxide poisoning can lead to cyanosis as well. Oxygen saturation levels measure oxygenation and should be assessed when cyanosis is present.

Clubbing (on slide) involves selective rounded enlargement of the end of the fingers. Clubbing is relatively painless, and associated with chronic conditions that result in hypoxemia (bronchiectasis, cystic fibrosis, and lung CA).

Regarding pain, inflammation of the parietal pleura can cause a sharp/stabbing pain with inspiration, which is exacerbated by laughing/coughing. A pleural friction rub may be heard over the painful area and can occur with issues such as PE, tracheitis, and bronchitis.
As we just discussed, hypercapnia is common with hypoventilation.
Causes of hypercapnia: 1) drugs that depress the respiratory system, 2) infections of CNS, and 3) spinal cord disruptions/injuries. Complications of hypercapnia include F&E imbalances and the potential for dysrhythmias.

Ischemia refers to decreased levels of oxygenation. Hypoxemia refers to a reduced oxygenation of arterial blood (PaO2) and reflects a respiratory alteration. Hypoxia refers to reduced oxygen within cells caused by conditions (not exclusive to respiratory dysfunction—e.g., low cardiac output).
Causes of hypoxemia: 1) poor oxygen delivery to alveoli, 2) poor delivery of O2 from the alveoli into the blood, and 3) poor perfusion of O2 within the pulmonary capillaries, which can lead to "shunting" which will be discussed on next slide. S/S: acute hypoxemia may include cyanosis, confusion, tachycardia, edema, and decreased renal output.


The top left image depicts a normal V/Q. An equal amnt of oxygenated and unoxygenated blood within the alveoli (reflects balanced ventilation-perfusion).

The image on the top right depicts poor ventilation...the narrowed area results in a "mismatch" that describes an abnormal (or low) ventilation-perfusion ratio.

The bottom left image reflects an imbalanced ventilation-perfusion ratio most common cause of hypoxemia. As the blood flows from the right side of the heart, to the lungs, to the left side....with shunting, unoxygenated blood bypasses the lungs and goes directly to the right side of the heart and into systemic circulation.

So, "shunting" refers to inadequate ventilation within the lung (common with issues such as atelectasis, asthma, and pulmonary edema) and is often associated with alveolar collapse. Poorly ventilated areas constrict, causing a right-to-left shunt in which venous blood is shunted into the arterial system without being oxygenated. Normally, less than 5% of cardiac output contains venous blood that has bypassed oxygenation. With a right-to-left shunt, even more venous blood is not oxygenated.
Pneumothorax is the presence of air or gas within the pleural space. It's often caused by a rupture of tissue surrounding the lung or within the pleura and chest wall. Air begins to separate the visceral and parietal pleura, destroying the negative pressure that keeps the lung inflated.

An open pneumothorax develops when air pressure in the pleural space = barometric pressure b/c air drawn into the pleural space during inspiration is forced back out during expiration.

A tension pneumothorax results when the site of pleural rupture acts as a one-way valve, permitting air to enter on inspiration, but not back out. As more air enters the space, pressure within begins to exceed barometric pressure. Eventually, the pressure builds up to compression atelectasis, which causes displacement of the mediastinum and heart (shift to the unaffected side). A tension pneumothorax is considered life threatening.

A spontaneous pneumothorax is as it sounds in that it occurs unexpectedly in healthy individuals (risk greater for men btwn ages of 20-40). Cause is unknown, but condition is r/t to the spontaneous rupture of blister-like formations on visceral pleura. The rupture can occur during sleep, rest, or exercise.

A secondary pneumothorax can be caused by 1) chest trauma (such as a rib fx or bullet wound) that tears the pleura, 2) ruptured blisters, and 3) mechanical ventilation.

*S/S (spontaneous or secondary pneumothorax): begin with sudden pleural pain, tachypnea, and dyspnea and vary depending on the size of the pneumothorax. Physical examination may reveal absent or decreased breath sounds and hyperresonance to percussion on the affected side. Tension pneumothorax may be complicated by severe hypoxemia, tracheal deviation away from the affected lung, and hypotension (low blood pressure). Deterioration occurs rapidly and immediate treatment is required. Diagnosis of pneumothorax is made with chest radiographs and computed tomography (CT
Breathing in toxic gases/agents such as smoke or ammonia can cause respiratory dysfunction (top image). Inhalation injuries from burns can occur from substances such as toxic gases and heat, causing damage and dysfunction for a number of breathing mechanisms. Inhalation of toxic gases can lead to complications such as ARDS and pneumonia. S/S: burning of the eyes, nose, and throat, coughing, chest tightness, and dyspnea (hypoxemia is common)

Keep in mind that oxygen is considered a drug....prolonged exposure to high concentrations can lead to oxygen toxicity, which causes a severe inflammatory response mediated by toxic oxygen radicals that damage the alveolocapillary membranes. These changes lead to decreased surfactant secretion, alveolar edema, and decreased lung compliance.

Pneumoconiosis represents any change in the lungs caused by inhalation of inorganic dust particles (occurs most commonly in the workplace). Pneumoconiosis usually occurs after years of exposure to the offending dust, which progressively leads to fibrosis of lung tissue. Common causes include silica, asbestos, and coal. Invasion of these foreign dust particles leads to chronic inflammation, scarring of the alveolar membrane, and results in pulmonary fibrosis and pulmonary deterioration. S/S: cough, chronic sputum production, dyspnea, decreased lung volumes, and hypoxemia.

Allergic alveolitis refers to the inhalation of organic dust (i.e., grains, bird droppings, feathers, etc), which results in an allergic inflammatory response. Repeated and prolonged exposure to the allergen results in lung inflammation. An acute occurrence causes fever, cough, and chills a few hours after exposure. In the subacute form, coughing and dyspnea are common and sometimes require hospitalization
Look at slide 21 pictures (ABCD).

Airway Obstruction Caused by Emphysema, Chronic Bronchitis, and Asthma.

A: The normal lung
B: Emphysema: illustrates enlargement and destruction of alveolar walls with loss of elasticity and trapping of air
C: Chronic bronchitis: inflammation and thickening of mucous membrane with accumulation of mucus and pus leading to obstruction; characterized by cough.
D: Bronchial asthma: thick mucus, mucosal edema, and smooth muscle spasm causing obstruction of small airways; breathing becomes labored, and expiration is difficult.

Chronic obstructive pulmonary disease (COPD) is defined as a preventable and treatable disease with potentially sig extrapulmonary effects that may contribute to the severity of symptoms experienced
Air trapping is a characteristic of COPD...the image on the left illustrates this mechanism. Mucous plugs and narrowed airways cause air trapping and hyperinflation of alveoli on expiration. During inspiration, the airways are pulled open, allowing gas to flow past the obstruction. During expiration, decreased elastic recoil of the bronchial walls results in collapse of the airways and prevents normal expiratory airflow.

Discuss patho of COPD thru image on right...

COPD is characterized by limited airflow that can not be reversed. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases.

RF: tobacco smoke (cigarette, pipe, cigar, and environmental tobacco smoke), occupational dusts and chemicals (vapors, irritants, and fumes), indoor air pollution from biomass fuel used for cooking and heating (in poorly vented dwellings), outdoor air pollution, and any factor that affects lung growth during gestation and childhood (low birth weight, respiratory tract infections). Thought to be a genetic link as well....
Emphysema refers to abnormal, permanent enlargement of gas-exchange airways, accompanied by destruction of alveolar walls. Obstruction results from changes in lung tissues (different from mucous production and inflammation of chronic bronchitis). A major characteristic of emphysema is loss of elastic recoil.

RF: thought to have a genetic component and secondary emphysema results from the inhalation of cigarette smoke, air pollution, and occupational exposures

Patho: begins with destruction of the alveolar and loss of elastic recoil of the bronchi. Alveolar destruction also produces large air spaces within and around lung tissue (known as bullae and blebs). Bullae and blebs are not effective for gas exchange and result in significant ventilation-perfusion mismatching and hypoxemia. Expiration becomes difficult because loss of elastic recoil reduces the volume of air that can be expired passively and air is trapped in the lungs. Air trapping causes hyperexpansion of the chest and places the muscles of respiration at a mechanical disadvantage. Results in increased workload of breathing, so many individuals develop hypoventilation and hypercapnia late within the course of the disease. Persistent inflammation in the airways can result in hyperreactivity of the bronchi with bronchoconstriction, which may be partially reversible with bronchodilators. Chronic inflammation can have significant systemic effects including weight loss, muscle weakness, and increased susceptibility to comorbidities, such as infection.

Let's compare some s/s...
First of all, Pneumonia is an infection within the lower respiratory tract caused by all kinds of microorganisms (bacterial, viruses, fungi, etc).
RF: older age, compromised immunity, and smoking. The causative microorganism influences how the individual presents clinically. Nosocomial infections refers to pneumonia that occurs during hospitalization. Community-acquired pneumonia is caused by Streptococcus pneumoniae, which sometimes results in hospitalization.

Aspiration of oropharyngeal secretions is the most common route of infection. Another route is through the inhalation of microorganisms that have been released into the air when an infected individual coughs, sneezes, or talks. Pneumonia can also result when bacteria is spread to the lungs in the blood from bacteremia that can result from infection elsewhere in the body.

Viral pneumonia is usually mild and self-limiting, but can set the stage for a secondary bacterial infection through the immunocompromised system. Viral pneumonia also can be a complication of another viral illness, such as chickenpox or measles (spread from the blood). Viruses destroy the ciliated epithelial cells and invade the goblet cells and bronchial mucous glands. Sloughing of destroyed bronchial epithelium occurs throughout the respiratory tract and bronchial walls become edematous and infiltrated with leukocytes. In severe cases, the alveoli are involved with decreased compliance and increased work of breathing.

S/S: fever, chills, productive or dry cough, malaise, pleural pain, and sometimes dyspnea and hemoptysis. Physical examination may show signs of pulmonary consolidation, such as dullness to percussion, inspiratory crackles, increased tactile fremitus, egophony (hoarseness), and whispered pectoriloquy. Individuals also may demonstrate symptoms and signs of underlying systemic disease or sepsis.

Tuberculosis (TB) is an infection caused by Mycobacterium tuberculosis, an acid-fast bacillus that usually affects the lungs. TB spreads easily and occurs commonly thru emigration of infected individuals from high-prevalence countries, transmission in crowded institutional settings (prisons), and homelessness (shelters).

Patho: TB is highly contagious and transmitted from person to person via airborne droplets. In healthy individuals, the microorganism is usually contained by the inflammatory and immune response systems, resulting in a latent infection. The latent form of TB is associated with no clinical evidence of disease. Microorganisms lodge in the lung periphery, usually in the upper lobe. Some bacilli migrate through the lymphatics and become lodged in the lymph nodes, where they encounter lymphocytes and initiate the immune response.

Patho for latent TB: Bacilli that are inspired into the lung multiply and cause localized inflammation, which causes activation of alveolar macrophages and neutrophils. These phagocytes engulf the bacilli, isolating it to prevent spread. The neutrophils and macrophages seal off the colonies of bacilli, forming a granulomatous lesion called a tubercle. Infected tissues within the tubercle die, forming cheese-like material called caesous necrosis. Scar tissue then grows around the tubercle, completing isolating the bacilli. The immune response is complete after about 10 days, preventing further multiplication of the bacilli. Once the bacilli are isolated in tubercles and immunity develops, tuberculosis may remain latent for life.

S/S: Latent TB is asymptomatic. Symptoms of active TB often develop gradually until the disease is advanced. S/S: fatigue, weight loss, lethargy, anorexia (loss of appetite), and a low-grade fever that usually occur in the afternoon. A cough that produces purulent sputum develops slowly and becomes more frequent over several weeks or months. Night sweats and general anxiety are often present. Dyspnea, chest pain, and hemoptysis may occur as the disease progresses.
Mean pulmonary artery pressure 5 to 10mmHg above normal or above 20mmHg
Primary pulmonary hypertension
-Idiopathic
Disease of the respiratory system and hypoxemia are more common causes.

Pulmonary atrial hypertension is defined as a mean pulmonary artery pressure >25 mm Hg and is classified into several categories:
Idiopathic, genetic, drug or toxin induced (weight loss medications, amphetamines, cocaine)
Left heart disease
Chronic lung disease, hypoxia, or both
Chronic thromboembolic pulmonary HTN
5. Or caused by other multifactorial mechanisms including blood, metabolic, and systemic disorders.

Patho: Idiopathic pulmonary arterial hypertension (IPAH) is characterized by endothelial dysfunction and overproduction of vasoconstrictors. Vascular growth factors are released, which cause remodeling within pulmonary smooth muscle. Fibrosis and vessel wall thickening occur, which causes luminal narrowing and a constriction of flow. These changes cause resistance to pulmonary artery blood flow, which increases the pressure in the pulmonary arteries. As resistance and pressure increase, the workload of the right ventricle increases and subsequent right ventricular hypertrophy, followed by right ventricular enlargement (cor pulmonale).

Classifcations: Pulmonary arterial hypertension, pulmonary venous hypertension, pulmonary hypertension due to a respiratory disease or hypoxemia. Pulmonary hypertension due to thrombotic or embolic disease. Pulmonary hypertension due to diseases of the pulmonary vasculature.

Pulmonary hypertension associated with lung disease, hypoxia, or both, is a serious complication of many acute and chronic pulmonary disorders, such as COPD, fibrosis, and hypoventilation associated with obesity. These conditions are complicated by hypoxic pulmonary vasoconstriction that further increases pulmonary artery pressures.

S/S: Initially, pulmonary hypertension may be seen on x-ray (thru enlargement of the right heart) or an ECG reflects right ventricular hypertrophy. Fatigue, chest discomfort, tachypnea, and dyspnea (particularly with exercise) are common. Examination may reveal peripheral edema, jugular venous distention, a precordial heave, and accentuation of the pulmonary component of the second heart sound
Most common cause is cigarette smoking. Heavy smokers have a 20 times greater chance of developing lung cancer than nonsmokers. Smoking is related to cancers of the larynx, oral cavity, esophagus, and urinary bladder. Environmental or occupational risk factors are also associated.
Lung cancers arise from the epithelium of the respiratory tract. The most common cause of lung cancer is tobacco smoking. Smokers with obstructive lung disease are at even greater risk. Other risk factors for lung cancer include secondhand smoke, occupational exposures to certain workplace toxins, radiation, and air pollution. Genetic risks include polymorphisms of the genes responsible for growth factor receptors, DNA repair, and detoxification of inhaled smoke.

Patho: tobacco smoke contains more than 30 carcinogens and is responsible for causing 80% to 90% of lung cancers. These carcinogens, along with a genetic component, result in multiple abnormalities in bronchial cells including deletions of chromosomes, activation of oncogenes, and inactivation of tumor-suppressor genes. The most common genetic abnormality associated with lung CA is loss of the tumor-suppressor gene. Once lung CA is initiated by these carcinogen-induced mutations, further tumor development is promoted by growth factors such as epidermal growth factor. Repetitive exposure of the bronchial mucosa to tobacco smoke leads to epithelial cell changes that progress from metaplasia to carcinoma in situ, and finally to invasive carcinoma. Further tumor progression includes invasion of surrounding tissues and finally metastasis to distant sites including the brain, bone marrow, and liver.

Image: A: Squamous cell carcinoma, B: Peripheral adenocarcinoma (the tumor shows prominent black pigmentation) and C: small cell carcinoma.


Characteristics of Lung Cancer: Tumor type: Squamous cell carcinoma. Growth rate: Slow. Metastasis: Late. Manifestatons: Cough, hempptysis, sputum production. Tumor type: Adenocarcinoma. Growth rate: Moderate. Metastasis: Early. Manifestations: Pleural effusion. Tumor type: Large cell carcinoma. Growth rate: Rapid. Metastasis: early. Manifestations: Chest wall pain, pleural effusion, cough, sputum production, hemoptysis. Tumor type: Small cell carcinoma. Growth rate: very rapid. Metastasis: Very early. Manifestations: Cough, cheset pain, dyspnea, hemoptysis, localized wheezing.
Diagnosis:

Squamous biopsy, sputum analysis, and bronchoscopy
Adenocarcinoma radiography and fiberoptic bronchoscopy
Large cell carcinoma sputum analysis and bronchoscopy
Small cell carcinoma radiography, sputum analysis, and bronchoscopy
Non-small cell lung cancer:

Squamous cell carcinoma is typically located near the hila and project into bronchi. Because of this central location, symptoms of nonproductive cough or hemoptysis are common. Pneumonia and atelectasis can accompany squamous cell carcinoma. Chest pain is a late symptom associated with large tumors. These tumors are often fairly well localized and tend not to metastasize until late in the course of the disease.

2) Adenocarcinoma (tumor arising from glands—image on slide) develops in a stepwise fashion through atypical adenomatous hyperplasia, adenocarcinoma in situ, and minimally invasive adenocarcinoma to invasive carcinoma. These tumors, which are usually smaller than 4 cm, more commonly arise in the peripheral regions of the pulmonary parenchyma. These tumors may be asymptomatic and discovered by routine chest roentgenogram in the early stages, or the individual may present with pleuritic chest pain and shortness of breath from pleural involvement by the tumor. They are slow-growing tumors with an unpredictable pattern of metastasis through the pulmonary arterial system and mediastinal lymph nodes.

3) Large cell carcinomas have lost all evidence of differentiation and are referred to as undifferentiated large cell anaplastic cancer. The cells are large and contain darkly stained nuclei. These tumors commonly arise centrally and can grow to distort the trachea and cause widening of the carina.

Small cell lung cancer:

1) Small cell carcinomas are the most common type of neuroendocrine lung tumors. Most of these tumors are central in origin. Cell sizes range from 6 to 8 μm (micrometers). Because these tumors show a rapid rate of growth and tend to metastasize early and widely, small cell carcinomas have the worst prognosis. Small cell carcinoma arises from neuroendocrine cells that contain neurosecretory granules; thus small cell carcinoma is often associated with ectopic hormone production. Ectopic hormone production is important to the clinician because resulting signs and symptoms (called paraneoplastic syndromes) may be the first manifestation of the underlying cancer. Small cell carcinomas most commonly produce antidiuretic hormone, resulting in the syndrome of inappropriate antidiuretic hormone secretion (SIADH). In other tumors, adrenocorticotropic hormone (ACTH) secretion leads to the development of Cushing syndrome. Signs and symptoms related to this condition include muscular weakness, facial edema, hypokalemia, alkalosis, hyperglycemia, hypertension, and increased pigmentation. Small cell lung cancer cells also can produce gastrin-releasing peptide and calcitonin.