Module 3: Structures/Functions of Respiratory System Flashcards
Primary Purpose of System
Primary purpose: gas exchange
Transfer of oxygen (O2) and carbon dioxide (CO2)
between atmosphere and blood
Two parts
Upper respiratory tract
Lower respiratory tract
Adequate O2 and a healthy, functioning respiratory system is necessary
Diagram of System
Upper Respiratory Track
Upper respiratory tract
Nose
* Warm, filter, humidify
* Septum
* Turbinates
Mouth
Pharynx
* Nasopharynx
* Oropharynx
* Laryngopharynx
Epiglottis
Larynx
Trachea
* 5” long X 1” wide
* Carina—bifurcation
* Angle of Louis
* Vigorous coughing
with suctioning
Lower Respiratory Tract
Lower respiratory tract
Bronchi
Bronchioles
Alveolar ducts
Alveoli
Primary site for gas
exchange with
pulmonary capillaries
Pores of Kohn
Interconnections
between alveoli
Allow air to pass; also
bacteria
Lung lobes
* Right—3
* Left—2
Hilus
* Entry of bronchi,
pulmonary vessels,
nerves into lungs
* R bronchus shorter,
wider, straighter than
left
* Aspiration more likely
in R lung
Bronchoconstriction
Bronchodilation
Trachea and bronchi—
anatomic dead space (VD);
no gas exchange
Bronchioles—smooth
muscle constricts and
dilates
Alveoli—end part of
respiratory tract; gases
exchange
Surfactant
Lipoprotein secreted by alveoli when stretched
Reduces surface tension to make alveoli less likely to
collapse
A sigh (slightly larger breath) occurs every 5-6
breaths stretches alveoli, promotes surfactant
secretion
Atelectasis—collapsed alveoli
Atelectasis refers to the collapse or closure of alveoli, which results in reduced gas exchange. It can occur in a part of the lung or the entire lung. This condition can be caused by various factors, such as blockage of the airways (e.g., by mucus or foreign bodies), pressure from outside the lung (e.g., tumor, fluid, or air in the pleural space), or lack of surfactant (as in neonatal respiratory distress syndrome). Atelectasis is common after surgery or in patients who have been bedridden for an extended period. It can lead to decreased oxygen levels in the blood and may predispose individuals to pneumonia.
Anesthesia: Anesthesia, particularly general anesthesia, can affect the respiratory system in several ways. During general anesthesia, patients are often unable to breathe on their own and require mechanical ventilation. Anesthesia can lead to a decrease in lung volume and a reduction in the natural surfactant production, which can predispose patients to atelectasis. Post-operative respiratory complications are common concerns, especially in surgeries involving the upper abdomen or thorax.
ARDS (Acute Respiratory Distress Syndrome): ARDS is a severe, life-threatening condition characterized by rapid onset of widespread inflammation in the lungs. It can be triggered by various factors, including severe infection (sepsis), trauma, pneumonia, and inhalation injuries. In ARDS, the alveolar-capillary barrier becomes damaged, leading to leakage of fluid into the alveoli, which impairs gas exchange and leads to decreased oxygen levels in the blood and difficulty breathing. ARDS is a medical emergency that requires hospitalization and often mechanical ventilation in an intensive care unit.
Blood Supply
Pulmonary Circulation (Gas Exchange):
Artery (Pulmonary Artery): Deoxygenated blood is pumped from the right ventricle of the heart into the pulmonary artery. This is somewhat unique as most arteries carry oxygenated blood, but in this case, the pulmonary artery carries blood that’s low in oxygen to the lungs.
Capillaries in the Lungs: These small blood vessels surround the alveoli (air sacs in the lungs). Here, the critical exchange of gases occurs. Oxygen from the air within the alveoli diffuses into the blood in the capillaries, while carbon dioxide from the blood diffuses into the alveoli to be exhaled.
Veins (Pulmonary Veins): After oxygenation, the blood travels from the capillaries into the pulmonary veins. These veins carry oxygen-rich blood back to the left atrium of the heart. From there, it will be pumped into the systemic circulation to deliver oxygen to the rest of the body.
Bronchial Circulation
Arteries (Bronchial Arteries): The bronchial arteries branch off from the aorta or other major arteries and provide oxygenated blood to the lung tissue itself, including the bronchi and bronchioles. Unlike pulmonary circulation, which is focused on gas exchange, bronchial circulation primarily supplies the lungs with nutrients and oxygen for their own metabolic needs.
Veins (Azygos Vein): Deoxygenated blood from the lung tissues is collected by the bronchial veins. Some of this blood drains into the pulmonary veins, but a significant portion also drains into the azygos vein. The azygos vein is a large vein running up the side of the thoracic spine, which ultimately empties into the superior vena cava. This returns the deoxygenated blood back to the heart, completing the circuit.
Chest Wall
Ribs (24 total) and sternum
* Thoracic cage—protect lungs and heart
Mediastinum
* Heart, aorta, and esophagus
Pleura
* Parietal—lines chest cavity
* Visceral—lines lungs
* Intrapleural space: 10 to 20 mL fluid provides
lubrication; facilitates expansion
* Empyema – bacterial infection - accumulation of pus in the pleural space. Usually a complication of a bacterial infection, stemming from pneumonia
Chest Wall
Chest wall
Diaphragm—major muscle of respiration
* Inspiration—contracts toward abdomen; increases
intrathoracic volume
* Works with intercostal and scalene muscles
* Innervated by right and left phrenic nerves; arise from
cervical vertebrae 3 to 5
* Complete spinal cord injuries above level of C3 causes
total diaphragm paralysis, dependence on mechanical
ventilation
Physiology of Respiration
Oxygenation—O2 from atmosphere to organs and
tissues
* Oxygen dissolved in plasma = Partial pressure of
oxygen in arterial blood (PaO2); normal 80 to 100 mm
Hg
* Oxygen bound to hemoglobin = Arterial oxygen
saturation (SaO2); normal greater than 95%
Diffusion—O2 and CO2 exchange at alveolar-capillary
membrane; move from high to low concentration until
equilibrium reached
Physiology of Respiration
Ventilation
Inspiration and expiration occur due to intrathoracic
pressure changes and muscle action
Dyspnea causes activation of muscles to aid in
breathing
Expiration—passive
* Elastic recoil—lungs return to original size after
expansion
Inhalation
This is an active process initiated by the diaphragm and the intercostal muscles.
When you inhale, the diaphragm (a large muscle located at the base of the lungs) contracts and moves downward, increasing the space in the thoracic cavity.
Simultaneously, the external intercostal muscles (located between the ribs) contract, elevating the ribs and sternum, which further increases the volume of the thoracic cavity.
This expansion reduces the intrathoracic pressure (pressure within the thoracic cavity) below the atmospheric pressure.
Due to this pressure difference, air flows into the lungs, filling the alveoli, where gas exchange will occur.
Dyspnea + Muscle Activation
Dyspnea, or difficulty breathing, can occur due to various reasons like respiratory diseases, strenuous exercise, or even anxiety.
In response to dyspnea, the body activates additional muscles (like the neck muscles) to aid in breathing. This is essentially an attempt to increase lung volume more effectively and improve air intake.
This is often seen as labored breathing and is a sign that the body requires more oxygen than the usual breathing mechanism can supply.
Expiration (Exhalation)
Expiration under resting conditions is generally a passive process.
During expiration, the diaphragm and external intercostal muscles relax. This causes the thoracic cavity to decrease in volume.
As the volume decreases, the pressure within the thoracic cavity increases, becoming higher than the atmospheric pressure.
The increase in pressure forces air out of the lungs.
Elastic recoil of the lungs plays a crucial role here. The lungs have a natural tendency to recoil due to their elastic properties (just like a stretched rubber band returning to its original shape). This recoil helps in pushing the air out of the lungs during expiration.
Compliance + Resistance
Compliance:
-Definition: Compliance in the context of lung physiology refers to the ease with which the lungs and chest wall can be expanded. Essentially, it’s a measure of the lung’s ability to stretch and expand.
-Factors Influencing Compliance: Two main factors influencing lung compliance are elasticity and elastic recoil of the lung tissue.
-Elasticity refers to the ability of the lung tissue to return to its original shape after being stretched.
-Elastic Recoil is the ability of the lungs to recoil or shrink back to their original size after being stretched or expanded.
Decreased Compliance: When lung compliance is decreased, the lungs are stiffer and harder to inflate. This can be due to factors like fibrosis, where the lung tissue becomes scarred and less elastic. Diseases such as pulmonary fibrosis or acute respiratory distress syndrome (ARDS) can lead to decreased compliance.
Increased Compliance: Increased compliance means the lungs are too easy to inflate and have difficulty recoiling back. This can occur in conditions like emphysema, where the elastic tissue of the lungs is damaged, making it hard for the lungs to expel air effectively.
Resistance:
Definition: Resistance in respiratory physiology refers to the opposition to airflow during inspiration and expiration. It is largely determined by the diameter of the airways.
-Factors Influencing Resistance: The primary factor influencing airway resistance is the airway diameter. Resistance increases if the airways are narrowed.
-Causes of Increased Resistance:
-Airway Constriction: Conditions such as asthma involve the constriction of airway muscles, leading to narrower airways and increased resistance.
-Airway Secretions: Excessive mucus or secretions, as seen in chronic bronchitis or during respiratory infections, can also narrow the airways and increase resistance.
Control of Respiration: Medulla
Medulla is respiratory center
The medulla oblongata is located in the lower part of the brainstem, just above the spinal cord. It’s a key area responsible for regulating various involuntary functions, including breathing.
The medulla contains neuron groups that are essential for the automatic control of breathing. These neurons generate rhythmic breathing patterns and adjust the rate and depth of breathing.
There are two main areas within the medulla that are involved in respiratory control: the dorsal respiratory group (DRG) and the ventral respiratory group (VRG). The DRG primarily controls the rhythm of quiet breathing, while the VRG is active during increased respiratory demand (like during exercise).
Response to Chemical and Mechanical Signals:
-The medulla’s respiratory centers are sensitive to chemical changes in the blood, such as the levels of carbon dioxide (CO2), oxygen (O2), and the pH (acidity level).
-Chemoreceptors located in the medulla (central chemoreceptors) and in the carotid and aortic bodies (peripheral chemoreceptors) detect these changes and send signals to the medulla.
-An increase in CO2 or a decrease in pH (indicating acidity) in the blood stimulates the medulla to increase the rate and depth of breathing, thus enhancing the expulsion of CO2 and helping to regulate blood pH.
-The medulla also receives mechanical feedback from the lungs and chest wall, which helps coordinate the breathing process.
-Impulse Transmission to Respiratory Muscles:
The medulla sends nerve impulses down the spinal cord and through nerves like the phrenic nerve to the respiratory muscles.
-The phrenic nerve innervates the diaphragm, which is the primary muscle of respiration. When the medulla signals the diaphragm to contract, it moves downward, enlarging the thoracic cavity and causing inhalation.
-Other nerves control the intercostal muscles, which also play a role in expanding and contracting the chest cavity during breathing.
Central Chemoreceptors
Chemoreceptors are specialized sensory receptors that respond to changes in the chemical composition of body fluids. In the context of respiratory physiology, they play a crucial role in monitoring the levels of carbon dioxide (PaCO2), hydrogen ion concentration (H+), and pH in the blood and cerebrospinal fluid (CSF).
Central Chemoreceptors in the Medulla:
-Central chemoreceptors are primarily located near the ventral surface of the medulla oblongata in the brainstem.
They are sensitive to changes in the pH and PaCO2 of the cerebrospinal fluid (CSF) surrounding the brain.
Response to Changes in H+ Concentration and pH:
-Acidosis (Increased H+ Concentration): When there is a high concentration of H+ ions in the blood, indicating acidosis, the central chemoreceptors stimulate an increase in respiratory rate (RR) and tidal volume (VT). This response enhances the exhalation of CO2, which is a key component of the body’s acid-base balance, helping to reduce the acidity of the blood.
Alkalosis (Decreased H+ Concentration): In contrast, when there is a lower concentration of H+ ions, indicating alkalosis, the chemoreceptors will result in a decreased respiratory rate and tidal volume. This reduces the exhalation of CO2, allowing the body to retain more CO2 and thereby increase the acidity of the blood, balancing the pH.
-Response to Changes in PaCO2:
Increased PaCO2: An increase in PaCO2 (partial pressure of carbon dioxide in arterial blood) leads to an increase in the production of carbonic acid (H2CO3). This, in turn, lowers the pH of the CSF. The central chemoreceptors respond to this decrease in pH by stimulating the respiratory center to increase the respiratory rate. This helps to expel more CO2 from the body, thereby reducing the H2CO3 concentration and correcting the pH imbalance.
Decreased PaCO2: Conversely, a decrease in PaCO2 results in reduced production of carbonic acid, leading to an increase in the pH of the CSF. The central chemoreceptors respond by decreasing the respiratory rate, which helps to retain CO2 in the body, thereby reducing the pH to a more normal level.
Peripheral Chemoreceptors
Peripheral chemoreceptors, specifically located in the carotid bodies and aortic bodies, play a critical role in respiratory control by sensing changes in the blood’s oxygen (PaO2), carbon dioxide (PaCO2), and pH levels. They complement the role of central chemoreceptors by providing additional regulatory mechanisms.
Peripheral Chemoreceptors - Carotid and Aortic Bodies:
Location: The carotid bodies are located near the bifurcation of the carotid arteries in the neck, while the aortic bodies are found along the aorta.
Function: These chemoreceptors are sensitive to changes in the arterial blood, particularly:
Decreased PaO2 (partial pressure of oxygen): They are primarily responsive to hypoxemia (low oxygen levels in the blood). When PaO2 falls, these receptors stimulate the respiratory center to increase the respiratory rate (RR), enhancing oxygen intake and carbon dioxide expulsion.
Decreased pH and Increased PaCO2: While less sensitive to changes in PaCO2 and pH compared to central chemoreceptors, peripheral chemoreceptors still respond to significant alterations in these parameters by increasing respiration
COPD
COPD and Respiratory Drive:
Chronic CO2 Retention: In chronic respiratory conditions like COPD, patients often have persistently elevated PaCO2 levels due to impaired lung function. Over time, their bodies adapt to these higher levels.
Blunted Response to CO2: This adaptation leads to a blunted respiratory response to increased PaCO2. In other words, for these patients, an increase in PaCO2 does not trigger an increase in respiratory rate as effectively as it would in healthy individuals.
Hypoxic Drive: Consequently, in advanced COPD, the body may rely more on the hypoxic drive for respiratory stimulation. This means that it’s the low oxygen levels (hypoxemia), rather than the high CO2 levels, that predominantly stimulate breathing.
Risks of Oxygen Therapy: This shift to hypoxic drive is crucial when considering oxygen therapy for COPD patients. Over-oxygenation can reduce their respiratory drive, potentially leading to respiratory failure.
Therefore, oxygen therapy in these patients must be carefully monitored to maintain a balance—providing enough oxygen for tissue needs without suppressing their respiratory drive.
Summary of Chemoreceptors/Role on O2
Mnemonic: “CAP HeRo, LOW”
**C - Central chemoreceptors:
A - Acid (High H+ concentration, Low pH): Respiratory Rate Increases.
P - PaCO2 (High Carbon Dioxide): Respiratory Rate Increases.
Low PaCO2 (Decreased Carbon Dioxide): Respiratory Rate Decreases.
**He - Peripheral chemoreceptors (Carotid and Aortic Bodies):
R - Reduced Oxygen (Low PaO2): Respiratory Rate Increases.
o - Other Factors (High PaCO2 and Low pH): Respiratory Rate Increases.
***LOW - Lowering Factors:
L - Low H+ concentration (High pH, Alkalosis): Respiratory Rate Decreases.
O - Over Oxygenation (High PaO2): In patients with chronic CO2 retention (like COPD), can lead to decreased respiratory drive.
W - Waning CO2 (Lower PaCO2 due to hyperventilation): Respiratory Rate Decreases.