Module 5 - Respiratory System

Question 1

The respiratory system can be divided int o what 2 structures?

Answer 1

conducting airways and respiratory tissues

Question 2

What are the levels of branching

Answer 2

Trachea, bronchi, bronchioles, alveoli

Question 3

Where is the site of gas exchange

Answer 3

The alveoli

Question 4

What cells are in the alveolar epithelium

Answer 4

Type I and II alveolar cells and macrophages. Type I alveolar cells are thing squamous cells that cannot divide and make up 95% of the surface area.

Type II alveolar cells are cuboidal cells, and are just as numerous but cover 5% of the surface area. They synthesize surfactant which decreases surface tension in the alveoli and allows for greater ease in lung inflation. Upon injury, type II cells are capable of proliferating into both type I and II cells.

Macrophages are responsible for removing offending substances from the alveoli.

Question 5

What happens during inspiration and expiration

Answer 5

During inspiration, air from the outside travels down the pressure gradient from the high pressure area outside the body into the low pressure area down inside the lungs. In order to lower pressure in the thoracic cavity, neurosignals will cause the intercostal muscles to move the ribcage outward and the diaphragm to move downwards. As the size of the thoracic cavity increases, the internal pressure will drop, and the air will flow into the body, through the brachial tree, and into the lungs.

During expiration, we breathe out to eliminate carbon dioxide. In order to move carbon dioxide out of the body and into the air, the thoracic cavity will decrease in size by relaxing the intercostal muscles and moving the diaphragm upwards, which will increase the pressure in the thoracic cavity. Thus, the air will move out of the lungs and out of the body.

Question 6

What occurs with the diaphragm during inspiration and expiration

Answer 6

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.

Question 7

What is lung compliance?

Answer 7

Lung compliance is the ability of the lungs to stretch, expanding its shape, and then return to it’s starting shape. The lung tissue has elastic fibers as part of the connective tissue to allow this expansion and recoil. If the lungs are not able to recoil, it can be difficult to exhale and if they become less compliant it can create stiffness making it difficult to stretch to accomodate air.

Question 8

What is tidal volume? (VT)

Answer 8

Tidal volume is the normal volume of air inhaled or exhaled with each breath, ~500mL

Question 9

What is the inspiratory reserve volume (IRV)

Answer 9

The inspiratory reserve volume is the amount of air that can be forcibly inspired after taking in a normal breath (VT), ~3100mL

Question 10

What is the expiratory reserve volume (ERV)

Answer 10

Expiratory reserve volume is the amount of air that can be forcibly exhaled after letting out a normal breath (VT), ~1200mL

Question 11

What is the residual volume (RV)

Answer 11

The residual volume is the air remaining in the lung after forced expiration, ~1200mL.

Question 12

What is vital capacity (VC) and how is it calculated

Answer 12

Vital capacity is the amount of air that can be exhaled following a maximum (forcible) inhalation, ~4800 mL
VC = VT + IRV + ERV

Question 13

What is inspiratory capacity (IC) and how is it calculated

Answer 13

Inspiratory capacity is the max amount of air that can be inhaled following a normal expiration, ~3600 mL
IC = VT + IRV

Question 14

What is functional residual capacity (FRC) and how is it calculated

Answer 14

Functional residual capacity is the amount of air that remains in the lungs after a normal expiration, ~2400 mL
FRC = RV +ERV

Question 15

What is the total lung capacity (TLC) and how is it calculated

Answer 15

Total lung capacity is the sum of all the lung volumes, ~6000 mL
TLC = IRV + VT + ERV + RV

Question 16

What are pulmonary function tests (PFTs)

Answer 16

Pulmonary function tests look at pulmonary flow rates in relation to time.

Maximum voluntary ventilation (MVV): the volume of air a person can move into and out of the lungs during maximum effort lasting 12-15 seconds

Forced vital capacity (FVC): the volume of air that can be quickly and forcefully exhaled following a full inspiration (total lung capacity) - it will be low in obstructive disease.

Forced expiratory volume (FEV): expiratory volume in a given time. FEV1 is the FEV exhaled in the first second of FVC. Also used for diagnosing obstructive lung disorders.

Forced inspiratory vital flow (FIF): measures the respiratory response during rapid maximal inspiration

Question 17

What is ventilation? Perfusion? Diffusion?

Answer 17

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.

Question 18

What is the difference between a shunt and dead air space?

Answer 18

A shunt is formed when blood moves from the pulmonary circulation (right side of the heart) to 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. In a physiologic shunt, blood moves through unventilated parts of the lung creating a mismatch of ventilation and perfusion.

Anatomic dead air space is the volume of air taken in that does not undergo gas exchange. This air would be found in the conducting airways to the terminal bronchioles. Alveolar dead air space are alveoli that are ventilated but not perfused (no blood flow). Physiologic dead air space is the sum of the anatomic and alveolar dead space.

Question 19

What is oxyhemoglobin

Answer 19

Oxyhemoglobin is the term used to describe when hemoglobin is bound with oxygen.

Question 20

What is affinity

Answer 20

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.

Each hemoglobin molecule can bind up to 4 molecules of oxygen and with each bound oxygen molecule, it change shape to make each consecutive oxygen molecule easier to bind. The affinity of hemoglobin for oxygen increases with hemoglobin saturation. As hemoglobin releases oxygen into the surrounding tissues, the affinity must decrease. Affinity is influenced by pH, carbon dioxide concentration, and body temperature. It binds more readily to oxygen as the blood pH increases 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.

Question 21

How is carbon dioxide transported in the blood?

Answer 21

Carbon dioxide is transported in the blood mostly as bicarbonate, also attached to hemoglobin, and sometimes as dissolved carbon dioxide.

The amount of dissolved CO2 and the level of bicarbonate in the blood influences the acid-base balance. Once diffused into the red blood cells, it can either combine with hemoglobin or form carbonic acid (CO2 + water). This process is catalyzed in the red blood cells because of an enzyme called carbonic anhydrase.

Question 22

How is breathing controlled?

Answer 22

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.

Breathing can be controlled by automatic regulation mechanisms by chemoreceptors and lung receptors. Chemoreceptors monitor blood levels of oxygen, carbon dioxide, and pH and adjusts ventilation rates accordingly. There are central chemoreceptors surrounded by cerebral spinal fluid in the brain that can sense changes in the blood PCO2 levels because CO2 from the blood diffuses into the CSF, freeing up hydrogen which then stimulates the chemoreceptors. And increase in PCO2 produces short term increase in ventilation. Peripheral chemoreceptors are located in the carotid and aortic bodies and they monitor arterial blood oxygen levels, however are not stimulated until PO2 levels fall below 60 mm Hg.

Lung receptors monitor breathing patterns and lung function.

Breathing can also be controlled by voluntary mechanisms giving temporary control of breathing in response to activities like speaking, singing, or holding breath.

Question 23

What are the characteristics of COPD including the disease pathology, clinical presentation, diagnosis, and treatment

Answer 23

Chronic Obstructive Pulmonary Disease (COPD) can manifest as emphysema or chronic bronchitis. It is a progressive and irreversible disease. The mechanisms that obstruct airflow include inflammation, fibrosis of the bronchial wall, increased mucus secretion, and decreased elastic fibers and alveolar tissue.

Emphysema is the enlargement of the airspaces after the terminal bronchioles because of destruction of the alveolar walls and associated capillaries. It decreases surface area for diffusion of oxygen and CO2 gases, and causes a loss of elastic recoil in the lungs.

The main causes of emphysema are smoking which triggers an inflammatory response. Neutrophils and macrophages release a proteolytic enzyme called elastase that damages and breaks down the elastic fibers in the lung tissues, which compromise the lungs recoil ability and compliance. Normally elastase is inhibited by the AAT enzyme, but smoking decreases the enzyme’s activity. The enlargement of the airspaces in the lungs means the alveoli can collapse and trap air in them, which leads to hyperinflation of the lungs - further stretching the tissue and causing a loss of elasticity. In hyperinflation there’s no more room in the alveoli to expand to take in new air and the trapped air is going to increase the CO2 concentration and lead to a lowering of the pH.

The signs and symptoms of emphysema include chronic hypoxia and hypercapnia, chronic cough, dyspnea, wheezing, barrel chest, pursed lip breathing, and respiratory distress. (Pink Puffer)

Chronic bronchitis is a productive cough that lasts for 3+ months for two or more consecutive years. It is mostly the product of smoking and inhaling irritants/pollutants as well as recurring infections.

With chronic bronchitis, the bronchial tree epithelium’s cilia becomes damaged - it no longer is able to properly move mucus out - and this increases mucus producing goblet cells, enlarged mucus glands, and squamous cell metaplasia. This can lead to excessive mucus production and retention which leads to trapped bacteria, bronchial wall thickening, and fibrosis. This leads to narrowing of the bronchioles that leads to obstruction.

The signs and symptoms of chronic bronchitis include chronic cough, purulent sputum, dyspnea, wheezing, hypoxemia, hypercapnia, cyanosis. (Blue Bloater)

Chronic bronchitis and emphysema is often seen concurrently.

COPD is diagnosed via spirometry, chest x rays, and lab tests to diagnose polycythemia or the increase in red blood cells due to hypoxia.

Treatment includes smoking cessation to decrease progression, bronchodilators, mucolytic agents, anti-inflammatory, and oxygen therapy.

Question 24

What is the leading risk factor for COPD

Answer 24

Smoking

Question 25

Describe asthma including risk factors, disease pathology, clinical presentation, diagnosis, and treatment

Answer 25

Asthma is a chronic obstructive respiratory disease caused by bronchospasm, mucous, and edema narrowing airways leading to increased resistance.

Its etiology can be a genetic influence (particularly in children) with an IgE hypersensitivity reaction or an environmental influence like respiratory infection, smoking, irritants/pollutants, stress, fatigue, endocrine changes, or weather/temperature changes.

The mechanism includes either a genetic or environmental factor triggering a hypersensitivity reaction. The early response includes mast cells releasing histamine and inflammatory mediators which create an inflammatory environment in the respiratory system which leads to edema, mucus plugs, and bronchospasms. This leads to airway obstructions and then the path of asthma.

The delayed response (6-24 hours) involves a cytokine release and eosinophil migration along with other cells of chronic inflammation. Their presence in the airways is going to cause destruction of the epithelium. The smooth muscle can have hyperplasia and it can cause narrowing of the airways and bronchial constriction.

The signs and symptoms of asthma include wheezing, breathlessness, chest tightness, sputum production, anxiety, tachypnea (increase in respiratory rate), acidosis, and hypoxia.

Diagnosis can be difficult because the patient might not be symptomatic when they’re with the clinician, but we can look for respiratory distress, pulsus paradoxus, wheezing enlongated expiratory phase, family history of hypersensitivities, and you can do labs to check for increased eosinophils, blood gas measurements of hypoxemia or hypercapnia, and peak expiratory flow rate.

Treatment includes elimination of the triggering allergen, bronchodilators, and anti-inflammatories.

Question 26

What is atopy

Answer 26

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.

Question 27

Describe pneumothorax including risk factors, disease pathology, clinical presentation, diagnosis, and treatment

Answer 27

Pneumothorax is the presence of air in the pleural space that causes a partial or complete collapse of the affected lung.

Spontaneous pneumothorax is from the rupture of an alveolus or an air filled bleb on the surface of the lung. The air moves from the outside into the pleural cavity after the rupture and the lung collapses because of its own recoil in the absence of the tension caused by the pressure gradient in the pleural space cavity. There is also traumatic pneumothorax caused by a penetrating injury. Additionally, tension pneumothorax is when air enters the pleural space but cannot exit such as a penetrating chest wound.

The signs and symptoms include chest pain, increased respiratory rate, and dyspnea. With tension pneumothorax, the structures will be shifted to the unaffected side - the trachea and mediastinum will be deviated outside of the midline.

Pneumothorax is diagnosed by chest xray or chest CT scan. Pulse oximetry and arterial blood gas can also determine blood oxygenation.

Treatment of pneumothorax includes repairing the wound, removing air via needle aspiration or drainage system, reduce obstructions or compressions, re-inflate the collapsed area, and oxygen administration if hypoxemia needs to be treated.

Question 28

Describe atelectasis including the risk factors, disease pathology, clinical presentation, diagnosis, and treatment

Answer 28

Atelectasis is incomplete expansion of the lung or portion of the lung due to airway obstruction, compression, pleural effusion, or decreased surfactant. Airway obstructions are common from mucus plugs or foreign objects that make it down into the bronchial tree. The air in the alveoli gets reabsorbed so there’s no further incoming air downstream of the obstruction, so the lung will collapse. External compression can be from a tumor or fluid mass in the pleural cavity.

Signs and symptoms include tachypnea, tachycardia, shortness of breath, cyanosis, hypoxemia, and a decrease in chest expansion.

Atelectasis is diagnosed by signs and symptoms and chest xray or chest CT scan.

Treatment is dependent 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. Oxygen administration, ambulation, deep breathing, and body positions that favor increased lung expansion are helpful treatments.

Question 29

What type of substance causes a pulmonary embolism?

Answer 29

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.

Question 30

Describe pulmonary embolism including the risk factors, disease pathology, clinical presentation, diagnosis, and treatment

Answer 30

Pulmonary embolism is when the pulmonary arterial bed is obstructed by a thrombus. It is most commonly caused by deep vein thrombosis, particularly in the lower extremities or pelvis. DVT is caused by immobility, traveling or sitting for many hours. It causes blood to pool in in the veins in the lower extremities so clotting factors don’t get diluted and the risk of a clot increases.

A thrombus in the vein breaks away and becomes an embolism. It’s going to continue to move into larger veins towards the heart and won’t really get stuck until the smaller arterial vessels. The embolism will either dissolve, fragment, or continue to grow. If it occludes an artery, lit leads to decreased surfactant in the alveoli and collapse of the lung. It it causes a vascular obstruction that’s large enough it can also cause an infarction and death of lung tissue.

Signs and symptoms: dyspnea, chest pain, tachycardia, feeling anxiety, cough, pleural effusion, leg edema

Diagnosed by xray and CT cans. In high risk patients, pulmonary angiography can be used - contrast dye is used along with xray to see blood flow through the lungs.

Treatment: anticoagulant and fibrinolytic drugs or surgery. Can use an umbrella filter to filter out emboli from systemic circulation and it blocks the emboli from making it to the heart and into the lungs.

Question 31

Describe ARDS (acute respiratory distress syndrome) including the risk factors, disease pathology, clinical presentation, diagnosis, and treatment

Answer 31

ARDS is an acute lung injury. It’s characterized by severe inflammation and pulmonary edema without fluid overload or abnormal cardiac function. It decreases compliance in the lungs and paraventilation and decreased oxygen levels.

It only takes 24-48 hours from an injury for ARDS to take place and the mechanism is similar to the inflammatory response. An injury causes a release of inflammatory mediators which cause the capillaries to become permeable and that will allow fluids to infiltrate into the interstitial space and then into the alveoli. This is going to lead to a very protein rich edematous fluid that’s going to lead to an osmotic fluid pooling more fluid into the space. Activated neutrophils will release products that damage the alveolar cell. There’s going to be damage to the surfactant releasing cells and that decreases surfactant, which can cause the alveoli to collapse. The fluid in collapse is going to inhibit gas exchange and decrease lung compliance, which will eventually affect lung ventilation. At first oxygen is not going to be able to cross the respiratory membrane efficiently, but CO2 will still be able to be expired because it is more soluble.

Patients first present with alkalosis, and with time the CO2 will eventually accumulate in the blood and that leads to acidosis.

Most common causes are shock, sepsis, and trauma. Also anaphylaxis, aspiration of gastric acids, pneumonia, drug overdose, near drowning, and leukemia.

Signs and symptoms include dyspnea, hypoxemia. If it progresses - hypotension, decreased urine output, and acidosis. Eventually ventricular fibrillation. Also retractions, crackles, restlessness, and tachypnea.

Diagnosis can occur with arterial blood analysis and with looking at blood pH.

Treatment: address the underlying cause, hypoxemia, and respiratory acidosis, intubation and mechanical ventilation. Some patients recover but some have permanent lung damage.

Question 32

Describe respiratory acidosis including the risk factors, disease pathology, clinical presentation, diagnosis, and treatment

Answer 32

The blood has a narrow pH range of 7.35-7.45. Acidosis is dropping below that range. If CO2 joins with water, it will create carbonic acid, which can disassociate into water+CO2 or bicarbonate + Hydrogen ions (H+). The H+ influences pH. So the body has a dynamic organ system that can eliminate or retain carbon (lungs) or eliminate or retain bicarbonate (kidneys).

Hypoventilation (hypercapnia) leads to CO2 accumulation and an increase in hydrogen ions, which leads to respiratory acidosis. Medullary chemoreceptors will pick up in the decrease in pH and increase the rate and depth of breathing to remove CO2 and that will cause a shift in our equation so the hydrogen ion concentration is reduced to restore pH.

Causes: If CNS disease or drug induced depression of the CNS - CNS is necessary for moving those respiratory muscles. If someone has impaired ventilatory movement - neuromuscular disease, chest injury, extreme obesity. Obstructive diseases like COPD, bronchitis, emphysema. Or cystic fibrosis.

Symptoms - can be difficult to diagnose based on symptoms because there can be underlying pathologies causing the acidosis with similar symptoms and signs. So in addition to the underlying disorder symptoms, dyspnea, somnolence, anxiety, confusion/delirium.

Diagnosis with a pH below 7.35 and a PCO2 above 45 mm Hg

Treatment: bronchodilators, oxygen, removal of obstruction, if too high potassium levels hyperkalemia treatment.