Module 5 quiz
How is carbon dioxide transported in the blood?
As dissolved carbon dioxide, attached to hemoglobin, as bicarbonate Mine: Carbon dioxide is transported in the blood in three forms: As dissolved carbon dioxide (10%) Attached to hemoglobin (30%) As bicarbonate (60%)
What is lung compliance? What factors affect it?
Lung compliance is the ease with which lungs can be inflated. Elastin, collagen, elastic recoil, and surface tension can affect lung compliance. Mine: Lung compliance is the ease with which lungs can inflate. For example, blowing up a new balloon is hard because it is noncompliant. In contrast, blowing up a balloon that has already been inflated is easier because it has become compliant. Thus, it takes more pressure to move air into a noncompliant lung than a compliant one. Lung compliance depends on multiple factors including overall water content and surface tension, as well as the amount of elastin and collagen fibers that are present.
What are the levels of branching?
Trachea, bronchi, bronchioles, alveoli
What cells are in the alveolar epithelium?
Type 1 and II alveolar cells, macrophages
Be familiar with the causes and manifestations of respiratory acidosis in Table 5.4.
Causes Manifestations Depression of Respiratory Center Blood pH, CO2, HCO3- Drug overdose pH decreased Head injury PCO2 (primary) increased Lung Disease HCO3- (compensatory) increased Bronchial asthma Neural Function COPD Dilation of cerebral vessels and depression of neural function Pneumonia Headache Pulmonary edema Weakness Respiratory distress syndrome Behavior Changes (confusion, depression, paranoia, hallucinations) Airway Obstruction, Disorders of Chest Wall & Respiratory Muscles Tremors Paralysis of respiratory muscles Paralysis Chest injuries Stupor and coma Kyphoscoliosis Skin: warm and flushed Extreme obesity Signs of Compensation: Acid urine Treatment with paralytic drugs Breathing air with high CO2 content
The respiratory system can be divided into what 2 structures?
Conducting airways and respiratory tissues
Describe what happens during inspiration and expiration:
During inspiration, air is drawn into the lungs as the respiratory muscles expand the chest cavity. During expiration, air moves out of the lungs as the chest muscles relax and the chest cavity becomes smaller.
What is oxyhemoglobin?
Oxyhemoglobin is the term to describe when hemoglobin is bound with oxygen.
What is pneumothorax?
Pneumothorax is the presence of air in the pleural space that causes partial or complete collapse of the affected lung.
Be familiar with the risk factors, disease pathology, clinical presentation, diagnosis, and treatment of pneumothorax.
Pneumothorax is the presence of air in the pleural space that causes a partial or complete collapse of the affected lung. There are three main types, ranging from when it can occur spontaneously (spontaneous pneumothorax), from trauma (traumatic pneumothorax) or as a tension pneumothorax, a life-threatening condition. Spontaneous pneumothorax is usually from rupture of an alveolus or an air-filled bleb, or blister, on the surface of the lung. In healthy people, these usually occur in tall boys and young men between 10 and 30 years of age. It is thought the difference in pleural pressure from the top to the bottom of the lung is greater in tall people and this difference in pressure contributes to the development of blebs. In people with lung disease, especially emphysema, trapping of gas can occur which leads to a pneumothorax. Traumatic pneumothorax is usually the result of a penetrating chest wound or rib fracture puncturing the lung. Hemothorax (collection of blood between the chest wall and the lung) may be present also. Medical procedures such as transthoracic needle aspirations, central line insertion, intubation, positive-pressure ventilation, and CPR may cause a traumatic pneumothorax. Tension pneumothorax occurs when air enters the pleural space but cannot exit, such as a penetrating chest wound. It can collapse the lung on the affected side and cause compression of mediastinal structures, which can be fatal. See Figure 5.10 for details. Figure 5.10 (Top) Air enters the chest during inspiration and exits during expiration in the case of an open pneumothorax. (Bottom) In tension pneumothorax, air enters the chest but cannot leave placing pressure on the mediastinal structures including the heart. Pneumothorax: Clinical Presentation The symptoms of pneumothorax depend on the severity of the disease process. A spontaneous pneumothorax may present with chest pain on the affected side, as well as increased respiratory rate and difficulty breathing. Breath sounds will be decreased or absent on the affected side. With a tension pneumothorax, the structures will be shifted to the unaffected side, as evidenced in Figure 5.10. The trachea and mediastinum will be deviated outside of midline. Heart rate will increase, but cardiac output will decrease because of the increase in intrathoracic pressure. There may be jugular neck vein distention, subcutaneous emphysema (presence of air in the subcutaneous tissues of the chest and neck that crackles when pressed on), and clinical signs of shock from the impaired cardiac function. Hypoxemia can result as the affected lung blood vessels vasoconstrict, and lung function is lost. Pneumothorax: Diagnosis and Treatment Pneumothorax is diagnosed by chest x-ray or chest CT scan. Pulse oximetry and arterial blood gas are important in determining blood oxygenation. Treatment depends on the severity of the pneumothorax. In a small spontaneous pneumothorax, the air usually reabsorbs on its own. Observation, supplemental oxygen, and serial chest x-rays may be the only necessary treatment. In larger instances, the air must be removed by needle aspiration or a closed drainage system with or without suction. Emergency treatment of a tension pneumothorax requires the immediate insertion of a large-bore needle or chest tube into the affected side, along with one-way valve drainage or continuous chest suction to aid in re-inflating the affected lung. To prevent reoccurrence, people should be instructed to avoid cigarette smoking, high altitudes, flying in a non-pressurized aircraft, and scuba diving.
Be familiar with the disease pathology, clinical presentation, diagnosis, and treatment of pulmonary embolism.
Pulmonary embolism (PE) occurs when a substance lodges in a branch of the pulmonary artery and obstructs blood flow. The embolism may be a thrombus (Figure 5.12), air accidentally injected into an intravenous infusion, fat from the bone marrow after a fracture or trauma, or amniotic fluid that enters the maternal circulation after rupture of membranes. Pulmonary embolism causes approximately 50,000 deaths per year in the United States. Figure 5.12 Pulmonary embolism found in the main pulmonary artery. A majority of pulmonary emboli are thrombi from deep vein thrombosis (DVT) in the lower and upper extremities. PE causes obstruction of blood flow, which leads to impaired gas exchange and vasoconstriction in the lungs. This can lead to pulmonary hypertension and right heart failure. Virchow triad are three factors that predispose people to venous thrombosis. These include venous stasis, venous endothelial injury, and hypercoagulability states. As a review from module 4, there are inherited hypercoagulability disorders that increase the risk of thrombosis (e.g. antithrombin III deficiency, protein C and S deficiencies, factor V Leiden mutation). Venous stasis and venous endothelial injury can result from prolonged bed rest or immobility, trauma, surgery, childbirth, fractures of the hip and femur, MI and CHF, cancer, and spinal cord injury. Pulmonary Embolism: Clinical Presentation The symptoms of PE depend on the size and location of the obstruction. The most common symptoms are chest pain, dyspnea, sometimes cough, and increased respiratory rate. Pleuritic pain can cause a worsening pain on inspiration. Impaired gas exchange can cause moderate hypoxemia. Small emboli in the peripheral branches may be asymptomatic unless the person is elderly or acutely ill. Massive emboli are often fatal. Pulmonary Embolism: Diagnosis and Treatment The diagnosis of PE can be made with a good history and physical, ABGs, venous thrombosis studies, troponin, D-dimer testing, lung scans, ECG, and helical chest CT scan. Lab and radiologic studies are done to rule out other causes of chest pain or dyspnea. Lower extremity ultrasonography and other venous studies are important to locate the cause of the PE. The D-dimer test measures plasma D-dimer, which is a degradation product of coagulation factors that have been activated due to a thromboembolic event. Troponin levels may be increased due to stretching of the right ventricle by a large pulmonary infarction. A ventilation-perfusion scan examines the lung segments for blood flow and distribution of the radiolabeled gas that has been injected and inhaled. Helical (spiral) CT can detect emboli in the proximal pulmonary arteries. Treatment involves anticoagulant therapy (Lovenox), or thrombolytic therapy (if indicated) for multiple or large emboli to restore pulmonary blood flow. Anticoagulants can also be used to prevent DVT or PE after major surgical procedures. Identifying people at risk is important for prevention. Increasing mobility and using compression stockings or intermittent pneumatic compression boots can prevent venous stasis.
What type of substance causes a pulmonary embolism?
The embolism may be a thrombus, air accidentally injected into an intravenous infusion, fat from the bone marrow after a fracture or trauma, or amniotic fluid that enters the maternal circulation after rupture of membranes.
Know the difference between a shunt and dead air space in Figure 5.6.
A shunt is formed when blood moves from the pulmonary circulation (right side of the heart) to the systemic circulation (left side of the heart) without being oxygenated. In an anatomic shunt, blood moves from the venous to the arterial side without moving through the lungs, as seen with congenital heart defects. In a physiologic shunt, blood moves through unventilated parts of the lung creating a mismatch of ventilation and perfusion. This is typically a result of a destructive lung disorder or heart failure. In summary, gas exchange depends on equal amounts of air and blood entering the lungs. A mismatch of ventilation and perfusion occurs with dead air space and shunt (Figure 5.6). Shunt has perfusion without ventilation, resulting in a low ventilation-perfusion ratio. This occurs in atelectasis and airway obstruction. Dead air space has ventilation without perfusion, resulting in a high ventilation-perfusion ratio. This would occur with a pulmonary embolism which restricts blood flow to a part of the lung. Some diseases have both impaired ventilation and perfusion, a prime example being chronic obstructive lung disease.
Where is the site of gas exchange?
Alveoli
Be familiar with the risk factors, disease pathology, clinical presentation, diagnosis, and treatment of asthma.
Asthma is a chronic respiratory disease characterized by airway obstruction, bronchial hyperresponsiveness, airway inflammation, and in some cases, airway remodeling. It is the most common chronic respiratory disorder among all age groups. Although prevalence is higher among racial and ethnic minorities, a more valid relationship may exist between socioeconomic status and increased asthma prevalence. Sixty to seventy-eight percent of people with asthma also suffer from allergic rhinitis. More than 25 million Americans have asthma. Atopy is the genetic tendency for developing IgE-mediated hypersensitivity reactions in response to environmental allergens. It is one of the strongest predisposing factors for developing asthma. IgE is the antibody responsible for causing allergic reaction and inflammation. Other risk factors include family history of asthma, allergies (including dust mites, pollen, mold, cockroaches, stings, or bites), antenatal exposure to tobacco smoke and pollution, gastroesophageal reflux disease, exercise, cold air, and being of African American or Puerto Rican descent. Small subsets of people with hypersensitivity have a triad of asthma, chronic rhinosinusitis, and nasal polyps. They also tend to have asthma attacks in response to taking aspirin and other NSAIDs. Infectious agents constantly enter the body via the respiratory system. The bronchi have several protective methods against these invaders. These include the following: Recruitment of inflammatory cells from the bloodstream into the bronchial wall, where they directly attack the invading organisms and secrete inflammatory chemicals that are toxic to the organisms Swelling of the bronchial wall Mucus secretion Constriction of the airway The fundamental defect in asthma is that, for reasons that are unclear, these inflammatory actions occur in the bronchi when no serious infection, toxin, or other inhaled threat to the body exists. Airway inflammation is caused by bronchial hyper-responsiveness to stimuli and recurrent episodes of respiratory symptoms which are usually associated with reversible airflow obstruction. There are three components: Airway inflammation (primary event) Airway hyperresponsiveness (secondary event) Airflow obstruction (secondary event) Inflammation results from complex interactions among many inflammatory cells and mediators, including eosinophil recruitment and airway edema. As such, inflammation is a direct response of the immune system to a trigger. Airway narrowing is due to many factors. As the airway walls thicken due to these inflammatory reactions, the amount of airway narrowing produced by a given amount of smooth muscle contraction in asthma is much greater than it is in a normal airway. Thus, even a small contraction of bronchial smooth muscle can lead to dramatic increases in airway resistance when the bronchial walls are already thickened from the actions of inflammatory cells and airway edema. At the cellular level, airway inflammation is caused by multiple inflammatory cells, including eosinophils, lymphocytes, and mast cells. Secreted by many of these cell types, cytokines also play a role in the chronic inflammatory response. Recent studies further suggest the T-helper 2 (T2H) cell response is exaggerated when children have frequent viral infections. When T2H cells are released, more IgE is produced, further predisposing the airways for an allergic reaction. Contact with a trigger stimulates the cascade of neutrophils, eosinophils, lymphocytes, and mast cells which causes epithelial injury. This causes airway inflammation, which further increases hyperresponsiveness and decreased airflow. As mast cells release histamine and leukotrienes, this causes major bronchoconstriction, inflammation, and mucus secretion. Mast cells can trigger multiple cytokine release, which causes even more airway inflammation. The contraction of the airways and subsequent swelling leads to further airway obstruction. The term airway remodeling refers to the development of specific structural changes in the airway wall in asthma accompanying long-standing and severe airway inflammation. Airway remodeling and fibrosis may be the cause of "fixed" airflow obstruction in asthma that is not reversible with steroids, bronchodilators, or both. Histologically, one will see hypertrophy of bronchial smooth muscle and deposition of subepithelial collagen. There is a thickening of the basement membrane of the bronchial epithelium. There is also edema and inflammatory infiltrate in the bronchial walls, with a prominence of eosinophils and mast cells. Asthma: Clinical Presentation Asthma attacks are usually a response to a trigger - respiratory infections, emotional stress, or weather changes. Symptoms of asthma range from wheezing, breathlessness, chest tightness, and cough that is typically worse at night and early morning. Lungs sounds often exhibit wheezing, primarily upon expiration. More serious attacks can present with accessory muscle usage (to help breath), distant breath sounds, increased shortness of breath, and often anxiety. During an attack, the airways narrow due to bronchospasm, edema of the bronchial mucosa, and mucus plugging. This leads to a prolonged expiration. Air becomes trapped in the alveoli. Alveolar ventilation is reduced, causing a mismatch of ventilation and perfusion. This leads to hypoxemia (low O2) and hypercapnia (high CO2). Asthma: Diagnosis and Treatment Diagnosis is made primarily by PFTs, along with history and physical exam. Spirometry can measure FVC and FEV1. Airflow obstruction will show a reduced FEV1 relative to predicted values and an FEV1/FVC ratio of < 70%. An increase in the FEV1 of ≥ 12% after administration of a bronchodilator is a diagnostic hallmark of asthma. Peak expiratory flow (PEF) is a valuable tool to measure flow rates that the patient can use at home. A patient records their best forced exhalation. They can use that measurement to compare and contrast with the readings obtained when they have symptoms. There are four stages of asthma for children older than 12 years and adults. These include intermittent, mild persistent, moderate persistent, and severe persistent. This classification is used to determine treatment and identify people at high risk of life-threatening asthma attacks. The stages are summarized in Table 5.2 below.
What is atelectasis?
Atelectasis is an incomplete expansion of a lung, or portion of lung, caused by airway obstruction or lung compression.
What is atopy?
Atopy is the genetic tendency for developing IgE-mediated hypersensitivity reactions in response to environmental allergens. It is one of the strongest predisposing factors for developing asthma.
Be familiar with the risk factors, disease pathology, clinical presentation, diagnosis, and treatment of atelectasis.
Atelectasis is an incomplete expansion of a lung, or portion of a lung, caused by airway obstruction or lung compression. Atelectasis can occur in a newborn, resulting from a lung that has never been inflated. It can also occur in infants with impaired lung expansion, as seen in respiratory distress syndrome. Atelectasis in an adult can be caused by a mucous plug in the airway, or compression by fluid (pleural effusion from congestive heart failure), tumor mass (cancer), exudate, or anything else causing obstruction. It can affect portions of the alveoli, lung segments, or an entire lung lobe (Figure 5.11). Figure 5.11 Atelectasis caused by airway obstruction (left) and compression of lung tissue (right) The risk of obstructive atelectasis is increased following surgery. Anesthesia, pain and pain medications, and immobility promote retention of bronchial secretions. Patients are encouraged to frequently cough, deep breathe, change positions, hydrate adequately, and ambulate early to prevent atelectasis. Atelectasis: Clinical Presentation Symptoms of atelectasis include tachypnea (rapid breathing), tachycardia, dyspnea, cyanosis, signs of hypoxemia, diminished chest expansion, decreased breath sounds, and intercostal retractions. If the collapsed area is large, the mediastinum and trachea shift to the affected side. In compression atelectasis, the mediastinum shifts away from the affected lung. Atelectasis: Diagnosis and Treatment Atelectasis is diagnosed by signs and symptoms and chest x-ray and/or chest CT scan. Treatment depends on the cause and extent of lung involvement. If possible, treatment will reduce the airway obstruction or lung compression, and re-inflate the collapsed area of the lung. Oxygen administration, ambulation, deep breathing, and body positions that favor increased lung expansion are helpful treatments.
Be able to differentiate between emphysema and chronic bronchitis; be familiar with the disease pathology, clinical presentation, diagnosis, and treatment of COPD.
COPD encompasses two disorders: emphysema and chronic bronchitis. People can have one or the other, but often these diseases overlap. Emphysema Emphysema is characterized by a decrease in lung elasticity, enlargement of the airspaces distal to the terminal bronchioles, and destruction of the alveolar walls and capillary beds as seen in Figure 5.7. Enlargement of the airspaces leads to hyperinflation of the lungs, causing the total lung capacity (TLC) to increase. Under the microscope, the lungs look like honeycombs: empty air spaces surrounded by alveolar membranes. Two consequences are decreased elastic recoil of the alveoli, and bronchioles are more likely to collapse. This leads to difficulty getting air out, which causes hyperinflation, air trapping, and less surface area for gas exchange. Figure 5.7 (A) Emphysema in left lung shows widespread destruction of pulmonary parenchyma; (B) emphysema in lung resulting from alpha-1 antitrypsin deficiency, shows enlarged airspaces and loss of alveolar walls. Again, the two main causes of emphysema are smoking, which causes lung injury, and ATT deficiency. Antitrypsin is an antiprotease enzyme that protects the lung from injury. Specifically, it protects the lungs from neutrophil elastase, which destroys the elastic tissue of the lungs. Cigarette smoke and other irritants initiate inflammatory cell activity within the lungs. This releases elastase and other proteases. With ATT deficiency, the body cannot defend itself against these proteases. With smoking, the antiprotease production may be inadequate to neutralize the damaging effects. Figure 5.8 depicts this process. Figure 5.8 Protease (elastase) - antiprotease (antitrypsin) mechanisms of emphysema. Smoking and inherited ATT deficiency destroy elastic fibers in the lung, leading to the development of emphysema. Chronic Bronchitis Chronic bronchitis is defined as airway obstruction of the major and small airways. It is most commonly seen in middle-aged men and results from chronic irritation from smoking and recurrent respiratory infections. A clinical diagnosis of chronic bronchitis can be made with a history of a chronic, productive cough for at least 3 consecutive months in at least 2 consecutive years. Usually, the cough has been present for years, with increasing acute exacerbations with purulent sputum. Chronic bronchitis manifests with hypersecretion of mucus in the large airways, along with hypertrophy of the submucosal glands in the trachea and bronchi. Histologically, it reveals a large increase in goblet cells, excess mucus production with plugging of the airway lumen, inflammatory infiltration, and fibrosis of the bronchiolar wall. Viral and bacterial infections are a common issue and are regularly detected in this population. COPD: Clinical Presentation COPD usually manifests itself in the fifth or sixth decade of life, with fatigue, exercise intolerance, cough, sputum production, or shortness of breath. The productive cough is usually worse in the morning. The shortness of breath worsens as the disease progresses. Frequent viral or bacterial infections are common, causing respiratory insufficiency and work absences. The late stages of COPD involve recurrent respiratory infections and chronic respiratory failure. The terms "pink puffer" and "blue bloater" have been used to differentiate emphysema from chronic bronchitis. Pink puffer is the term for people with predominantly emphysema. It refers to the lack of cyanosis, the use of accessory muscles, and pursed-lip (puffer) breathing. Since there is a loss of lung elasticity and hyperinflation of the lungs, the airways often collapse during expiration due to higher pressure in the surrounding lung tissues. As air becomes trapped in the alveoli and lungs, the anteroposterior dimension of the chest becomes bigger - referred to as barrel chest (Figure 5.9). Patients may have a prolonged expiratory phase because of the obstruction to expiration. Breath sounds may have wheezing or be diminished throughout, and the patient becomes prone to diaphragmatic fatigue and acute respiratory failure. Figure 5.9 Normal chest wall versus barrel-shaped chest wall, characteristic of emphysema Blue bloater is the term used to describe those with chronic bronchitis. It refers to cyanosis and fluid retention common with right-sided heart failure. Clinically, the differentiation between the two diseases is difficult, as most people have some degree of both emphysema and chronic bronchitis. Changes in respiratory function due to airflow obstruction is the most common feature. Expiration (rather than inspiration) becomes more difficult. Exertional dyspnea, increased effort to breathe, heaviness, air hunger, or gasping are common symptoms. Activities involving the arms, especially above the shoulders, becomes very difficult due to the person needing to brace themselves to breathe. On auscultation, the expiratory phase is increased, and expiratory wheezes and crackles can be heard. As the disease worsens, people may use the tripod position to help breath. This describes sitting or standing while leaning forward to support the upper body with hands on the knees. It optimizes respiration by using the accessory muscles of the neck and upper chest to get more air into the lungs. Pursed-lip breathing also helps with airflow. Eventually, hypoxemia, hypercapnia, and cyanosis develop due to an imbalance of ventilation and perfusion. Severe hypoxemia, with an arterial PO2 level below 55 mm Hg, causes reflex vasoconstriction of the pulmonary vessels. It is more common in patients with chronic bronchitis type of COPD. Hypoxemia stimulates red blood cell production, causing polycythemia. The vasoconstriction causes an increase in pulmonary artery pressure, causing the right ventricle to work harder, which leads to right-sided heart failure with peripheral edema (cor pulmonale). COPD is diagnosed based on history, physical exam, PFTs, chest x-ray, and lab tests. The FVC is prolonged and decreased. FEV1 is decreased as well. Notably, a decreased FEV1/FVC ratio differentiates obstructive from restrictive diseases. RV and TLC are also increased. Spirometry is used to diagnose and stage disease severity. As the disease progresses, exercise tolerance, nutritional status, hemoglobin saturation, and arterial blood gases become important measurements. COPD: Treatment COPD treatment depends on the severity of the disease. Smoking cessation is the only treatment that slows the progression of the disease. Often an interdisciplinary approach is helpful to meet the various physical and psychosocial needs the patient and his or her family may have. Respiratory tract infections should be avoided if possible and treated accordingly. Patients should have both the pneumococcal and annual influenza vaccinations. Pulmonary rehabilitation programs have been proven to reduce hospitalizations and add to the quality of life in these patients. The primary pharmacologic treatment includes the use of inhaled short and long-acting bronchodilators, which relax the airway smooth muscle. Inhaled corticosteroids may be used in later disease but are not as useful as they are in asthma treatment. Oxygen therapy is prescribed when the PO2 levels drop under 55 mm Hg. Oxygen has been shown to reduce dyspnea and pulmonary hypertension and improve activity tolerance. The goal of oxygen therapy is to keep oxygen saturation to at least 90%.
What is the leading risk factor for COPD?
Smoking
How is breathing controlled?
The automatic regulation is controlled by both chemoreceptors and lung receptors. Chemoreceptors monitor blood levels of oxygen, carbon dioxide, and pH and adjusts ventilation accordingly. Lung receptors monitor breathing patterns and lung function. Mine: Chemoreceptors monitor blood levels of oxygen, carbon dioxide, and pH and adjusts ventilation rates accordingly. Lung receptors monitor breathing patterns and lung function. Voluntary regulation gives temporary control of breathing in response to various activities such as speaking, singing or holding breath while underwater.
Be familiar with the disease pathology, clinical presentation, diagnosis, and treatment of ARDS.
ARDS: Clinical Presentation ARDS presents with a rapid onset of respiratory distress (usually within 12-18 hours of triggering event), increased respiratory rate, and signs of respiratory failure. Hypoxemia occurs and is coupled with multiple organ failure. ARDS: Diagnosis and Treatment A chest x-ray will show diffuse bilateral infiltrates of the lungs from fluid ("white-out"), with normal cardiac function. Treatment focuses on supportive care of oxygen and ventilator support until the lungs heal and the underlying cause is addressed. Recovery may be complicated by lung scarring and fibrosis.
Be familiar with the conditions that can cause ARDS in Table 5.3.
Acute respiratory distress syndrome (ARDS) can be caused by several different conditions. The more prominent ones are summarized in Table 5.3. Table 5.3 Conditions in which ARDS can develop Aspiration Near drowning, aspirating gastric contents Drugs, Toxins, and Therapeutic Agents Free-base cocaine smoking, heroin, inhaled gases (smoke, ammonia), breathing high concentrations of oxygen, radiation Infection Septicemia Trauma and Shock Burns, fat embolism, chest trauma Disseminated intravascular coagulation Multiple blood transfusions Though these conditions are diverse in nature, they all lead to similar pathologic lung changes. These include diffuse epithelial cell injury with increased permeability of the alveolar-capillary membrane as seen in Figure 5.13. This allows fluid, protein, cellular debris, platelets, and blood cells to move out of the vascular compartment and into the interstitium and alveoli. Activated neutrophils release products that damage the alveolar cell and lead to edema, surfactant inactivation, and formation of a hyaline membrane that is resistant to gas exchange.
What are the characteristics of asthma?
Asthma is a chronic respiratory disease characterized by airway obstruction, bronchial hyperresponsiveness, airway inflammation, and in some cases, airway remodeling. Mine: Asthma attacks are usually a response to a trigger - respiratory infections, emotional stress, or weather changes. Symptoms of asthma range from wheezing, breathlessness, chest tightness, and cough that is typically worse at night and early morning. Lungs sounds often exhibit wheezing, primarily upon expiration. More serious attacks can present with accessory muscle usage (to help breath), distant breath sounds, increased shortness of breath, and often anxiety. During an attack, the airways narrow due to bronchospasm, edema of the bronchial mucosa, and mucus plugging. This leads to a prolonged expiration. Air becomes trapped in the alveoli. Alveolar ventilation is reduced, causing a mismatch of ventilation and perfusion. This leads to hypoxemia (low O2) and hypercapnia (high CO2).
Be familiar with the lung volumes, lung capacities, and pulmonary function tests in Figure 5.5.
Lung volumes refers to the amount of air exchanged from a single event during ventilation, either from inhaling or exhaling. Lung volumes can be categorized into four main components, of which three can be directly measured using spirometer: Tidal volume (VT) is the normal volume of air inhaled (or exhaled) with each breath, ~500 mL. Inspiratory reserve volume (IRV) is the amount of air that can be forcibly inspired after taking in a normal breath (VT), ~3100 mL. Expiratory reserve volume (ERV) is the amount of air that can be forcibly exhaled after letting out a normal breath (VT), ~1200 mL. Residual volume (RV) is the air remaining in the lung after forced expiration, ~1200 mL. However, residual volume cannot be directly measured with a spirometer. Instead, RV can be calculated through indirect methods. Lung capacities are calculated using lung volumes (above), both of which are measured independent of the duration. Whereas lung volumes each account for only a single function (either an inspiration or expiration event), lung capacities encompass two or more lung volumes. Vital capacity (VC) is the amount of air that can be exhaled following a maximum (forcible) inhalation, ~4800 mL. Thus, VC = VT + IRV + ERV Inspiratory capacity (IC) is the max amount of air that can be inhaled following a normal expiration (VT), ~3600 mL. Thus, IC = VT + IRV. Functional residual capacity (FRC) is the amount of air that remains in the lungs after a normal expiration (VT), ~2400 mL. Thus, FRC = RV + ERV. Total lung capacity (TLC) is the sum of all the lung volumes, ~6000 mL. Thus, TLC = IRV + VT + ERV + RV Pulmonary function tests (PFTs) look at pulmonary flow rates in relation to time. These include maximum voluntary ventilation, forced vital capacity, forced expiratory volumes and flow rates, and forced inspiratory flow rates. PFTs are used to diagnose respiratory disease or to work up respiratory complaints, or as a pre-op anesthesia or surgical risk evaluation. They are summarized below: Maximum voluntary ventilation (MVV): measures the volume of air a person can move into and out of the lungs during maximum effort lasting for 12-15 seconds. This measurement is converted to liters per minute. Forced vital capacity (FVC): measures the volume of air that can be quickly and forcefully exhaled following a full inspiration (to total lung capacity). FVC will be lower in obstructive disease. Forced expiratory volume (FEV): measures expiratory volume in a given time. FEV1 is the FEV exhaled in the first second of FVC. FEV is also useful in diagnosing obstructive lung disorders. Forced inspiratory vital flow (FIF): measures the respiratory response during rapid maximal inspiration.
Be familiar with the disease pathology, clinical presentation, diagnosis, and treatment of respiratory acidosis.
Respiratory acidosis occurs in conditions that impair alveolar ventilation. It causes an increase in plasma PCO2, called hypercapnia, and a decrease in pH. The most common cause of respiratory acidosis is decreased ventilation. It can occur in both acute or chronic conditions. Common causes and manifestations are summarized in Table 5.4 below. Respiratory acidosis can be due to acute disorders of ventilation, such as in narcotic overdose, lung disease, chest injury, weakness of the respiratory muscles, or airway obstruction. It can be caused by chronic disorders of ventilation, such as COPD. In people on oxygen therapy, it becomes vital not to supplement with too much oxygen. Their medullary respiratory center has adapted to the elevated CO2 levels and no longer responds to increases in PCO2. Therefore, a decrease in PO2 becomes the stimulus for respiration. If oxygen is given at too high of a rate, it suppresses the stimulus and the respiratory drive. Finally, increased carbon dioxide production can cause respiratory acidosis. It can result from exercise, fever, sepsis, and burns. In healthy individuals, an increase in CO2 is counteracted by an increase in CO2 elimination in the lungs. However, in people with lung diseases, they may not be able to eliminate the excess. Respiratory Acidosis: Clinical Presentation Symptoms typically depend on the cause and whether it is acute or chronic. Symptoms will present similar to hypoxemia. Since CO2 crosses the blood-brain barrier, it causes vasodilation and subsequent headache, blurred vision, irritability, muscle twitching, and psychological manifestations. Respiratory Acidosis: Diagnosis and Treatment Respiratory acidosis is diagnosed with a pH below 7.35 and a PCO2 above 45 mm Hg. Treatment is aimed at improving ventilation; in some cases, mechanical ventilation is needed.
What is affinity?
The ability of the hemoglobin molecule to bind oxygen in the lungs and release it in the tissues depends on the affinity of the molecule. Mine: The affinity of the hemoglobin molecule is the degree to which it is able to bind oxygen. Each hemoglobin molecule can bind up to four molecules of oxygen when fully saturated. After the first oxygen is bound, it changes shape to make each consecutive oxygen molecule easier to bind. Therefore, the affinity of hemoglobin for oxygen increases with hemoglobin saturation. As hemoglobin must not only bind but also release oxygen into the surrounding tissues, the affinity must decrease. Opposite to the binding sequence, the affinity decreases with each passing release of oxygen. Hemoglobin's affinity for oxygen is also influenced by pH, carbon dioxide concentration, and body temperature. It binds more readily to oxygen as the blood pH increases (> 7.45), and under conditions of decreased body temperature and CO2 concentration. Conversely, hemoglobin releases oxygen more readily in conditions of decreased pH (acidosis), increased CO2 concentration, and fever.
What occurs with the diaphragm during inspiration and expiration?
The diaphragm is the main muscle of inspiration. When the diaphragm contracts (inspiration), the chest expands. Upon expiration, the chest cavity decreases and pressure inside increases.
What are the characteristics of COPD?
The pathogenesis of COPD includes inflammation and fibrosis of the bronchial wall, hypertrophy of the submucosal glands and hypersecretion of mucus, and loss of elastic lung fibers and alveolar tissue. This airflow obstruction causes a mismatch in ventilation and perfusion. Alveolar tissue destruction leads to a decreased surface area for gas exchange.
What is ventilation? Perfusion? Diffusion?
Ventilation is the movement of gases into and out of the lungs. Perfusion is the process that allows blood flow to help facilitate gas exchange. Diffusion is the movement of gases across the alveolar-capillary membrane. Mine: Ventilation - the flow of gases into and out of the alveoli of the lungs Perfusion - the flow of blood in the adjacent pulmonary capillaries Diffusion - the transfer of gases between the alveoli and the pulmonary capillaries
