MindMap Gallery Breathing mind map
This is a mind map about breathing, including resistance to pulmonary ventilation, indicators of pulmonary ventilation function, regulation of respiratory movements, etc.
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This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about plant asexual reproduction, and its main contents include: concept, spore reproduction, vegetative reproduction, tissue culture, and buds. The summary is comprehensive and meticulous, suitable as review materials.
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breathe
The power of pulmonary ventilation
Principles of pulmonary ventilation
Definition: The process of gas exchange between the lungs and the external environment
Pulmonary ventilation power
Direct power: the pressure difference between intrapulmonary pressure and atmospheric pressure
Motive force: rhythmic respiratory movement caused by contraction and relaxation of respiratory muscles
respiratory movements
Concept: Rhythmic expansion and contraction of the thorax caused by contraction and relaxation of respiratory muscles
Inhale
inspiratory muscles
Main respiratory muscles: diaphragm, external intercostal muscles
Accessory respiratory muscles: scalenes, sternocleidomastoid
Inhalation process: contraction of diaphragm and external intercostal muscles → expansion of thorax → expansion of lung volume → reduction of intrapulmonary pressure → inhalation
exhale
Expiratory muscles: internal intercostal muscles, abdominal muscles
During expiration, the diaphragm and external intercostal muscles relax → the lungs elastically recoil and the volume decreases → the thorax shrinks → the intrapulmonary pressure increases → the gas is discharged → exhale
Breathing exercise patterns
Classified by breathing depth
Quiet breathing: Breathing movement in a quiet state, active inhalation and passive exhalation
Forced breathing: Deep and powerful breathing exercises during exercise, hypoxia, or increased CO₂. Inhalation becomes active, and exhalation becomes active as well.
Dyspnea: Under certain pathological conditions, not only breathing deepens and accelerates, but also symptoms such as nose flaring occur, accompanied by an uncomfortable feeling of trapped pressure in the chest.
Classification by respiratory performance
Chest breathing: intercostal muscles dominate, chest wall rises and falls
Abdominal breathing: diaphragm dominant, abdominal wall undulating
Mixed breathing: normal diaphragm and intercostal muscles are involved
intrapulmonary pressure
Definition: pressure within the alveoli, normal ±1-2mmHg
Influencing factors: Breathing speed, depth, and airway patency. When the airway is not clear, inhalation can reach -100~-30mmHg, and exhalation can reach 90~140mmHg.
Artificial respiration: Using artificial methods to create a pressure difference between the intrapulmonary pressure and the external air to maintain lung ventilation. Such as mouth-to-mouth artificial respiration, rhythmically raising the arms to press the back or squeezing the chest, and positive pressure ventilation with a ventilator.
intraperitoneal pressure
Peritoneal cavity: A closed potential space between the parietal and visceral layers of the pleura, containing a small amount of serous fluid.
serous action
Lubrication: Reduce the friction between the visceral wall and pleura during breathing
Adhesion effect: relying on the cohesion of liquid molecules to couple the movement of the thorax and lungs
Once the airtightness of the pleural cavity is destroyed, such as pneumothorax, the cohesion is destroyed and the lungs and thorax lose their coupling.
intrathoracic pressure
Definition: The pressure within the pleural cavity, usually negative pressure.
End of inspiration: -5~-10mmHg, end of expiration -3~-5mmHg
generation of intrathoracic pressure
Intrathoracic pressure = intrapulmonary pressure - elastic recoil of the lungs, intrapulmonary pressure during quiet breathing ≈ atmospheric pressure (760mmHg), ∴ intrathoracic pressure = - elastic recoil of the lungs
When coughing, sneezing, or holding one's breath and breathing forcefully, the intrapulmonary pressure increases significantly, which can be positive pressure.
The physiological significance of intrathoracic negative pressure
Keep the lungs in an expanded state
Promote venous and lymphatic return.
resistance to pulmonary ventilation
Elastic resistance and compliance
elastic resistance
The force of elastic tissue that resists deformation caused by external forces. That is, the tendency of the thorax and lungs to resist deformation and return. Compliance is generally used to measure elastic resistance. It is the main resistance during calm breathing and exists even without airflow. It is a static resistance.
Lung elastic resistance:
Inspiratory resistance, expiratory power
The elastic resistance of the lung tissue itself (1/3): produced by the elastic fibers and collagen fibers contained in the alveolar walls. Reduced in emphysema
Alveolar surface tension (2/3): generated by the liquid-air interface in the alveoli.
Elastic resistance of the thorax: The thorax is a two-way elastic body. The normal position of the thorax is 67% of its maximum volume, which is equivalent to the end of quiet breathing. Can be enlarged due to obesity, thoracic deformity, pleural thickening, etc.
Compliance
Definition: The ease with which elastic tissue expands under external force is inversely proportional to elastic resistance.
Compliance is a measure of elastic resistance, usually measured as "volume change per unit pressure change"
C=△V/△P
Lung compliance = lung volume change/transpulmonary pressure, normal 0.2L/cmH₂O
Thoracic compliance = chest volume change/transmural pressure, normal 0.2L/cmH₂O
Surface tension: shrinks the alveoli and generates alveolar retraction pressure. According to Laplace's law, P=2T/r, where T is the surface tension coefficient, that is, the surface tension per unit length.
surfactant
A mixture of lipoproteins produced by alveolar type II cells (large alveolar cells), 60% of which is dipalmityl lecithin or dipalmitoyl lecithin (DPPC). It can reduce the alveolar surface tension and is called pulmonary surfactant; 10% is surfactant binding protein (SP)
physiological significance
Reduce inspiratory resistance and facilitate lung expansion
Stable alveolar volume. Prevent excessive expansion of large alveoli and excessive shrinkage of small alveoli
Keep the alveoli "dry" to prevent pulmonary edema. (Reduce surface tension and prevent capillary plasma fluid from penetrating into the alveoli)
inelastic resistance
Accounting for 30%, it is dynamic resistance
Classification
Inertial resistance: the force that prevents lung ventilation due to the inertia of the airflow and tissues when the airflow is started, changed speed, and reversed. During calm breathing, the breathing frequency is low, the air flow speed is slow, and the inertial resistance is small and can be ignored.
Viscous resistance: The friction that occurs when tissues move relative to each other during breathing.
airway resistance
Definition: It comes from the friction between gas molecules and between gas molecules and the airway wall when the gas flows through the respiratory tract. It is the main component of flight elastic resistance, accounting for about 80% to 90%. Mainly distributed in the upper respiratory tract: 50% of the nose, 25% of the glottis, 25% of the tracheobronchi, and 10% of the bronchioles and below.
the main factor of influence
Air flow speed: high flow speed and high resistance
Air flow form: laminar flow, low resistance; turbulent flow, high resistance
Effect of airway radius
Airway transmural pressure: intra-airway pressure, intrathoracic negative pressure↑→tube diameter↑
outward traction of pulmonary parenchymal fibers
Autonomic nerve: Sympathetic nerve excitement → diameter ↑; Parasympathetic nerve excitement → diameter ↓
Chemical factors: Catecholamines, PGF₂α, PGF₂, LTB, histamine, CO₂.
Indicators of pulmonary ventilation function
Basic lung volume and lung volume
Tidal volume (TV): The amount of gas inhaled or exhaled with each breath, about 5000ml in quiet breathing, up to lung capacity
Inspiratory supplementary volume (IRV): the amount of gas that can be inhaled at the end of a calm inhalation and then inhaling as hard as possible, about 1500-2000ml
Expiratory supplementary volume (ERV): The amount of gas that can be exhaled at the end of a calm expiration and then exhaling as hard as possible, about 900-1200ml
Residual volume (RV): The amount of gas that remains in the lungs at the end of maximum expiration and cannot be exhaled, about 1000-15000ml. Emphysema, lungs and bronchial tubes increase in size during asthma.
Inspiratory volume (IC): the maximum amount of air that can be inhaled at the end of a quiet inhalation.
Functional residual volume (FRV): The amount of gas that remains in the lungs at the end of quiet expiration and is not exhaled, about 2500ml, which can buffer the changes in alveolar gas PO₂ and PO₂ during breathing.
Vital capacity (VC): The maximum amount of air that can be exhaled from the lungs after inhaling as hard as possible. Reflects the maximum ventilation capacity of the lungs. The normal amount is 3500ml for men and 2500ml for women. Affected by many factors such as age, gender, and body shape.
Forced vital capacity (FVC): The maximum amount of air that can be exhaled from the lungs after one maximum inhalation and then exhaling as fast as possible.
Forced expiratory volume (FEV): After one maximum inhalation, try your best to exhale quickly, and record the amount of air exhaled at the end of 1, 2, and 3 seconds. Normally, it accounts for 80%, 96%, and 99% of FVC.
Pulmonary ventilation and alveolar ventilation.
pulmonary ventilation
Pulmonary ventilation: The total amount of gas inhaled or exhaled per minute, equal to tidal volume × respiratory rate, about six to nine liters in quiet breathing.
Percentage of ventilation reserve = maximum voluntary ventilation - quiet ventilation per minute / maximum voluntary ventilation × 100%, normal is above 93%, expressing the reserve capacity of ventilatory function
Maximum voluntary ventilation: Try to breathe deeply and quickly. The maximum volume of air that can be inhaled or exhaled per minute can generally reach 150 liters per minute, which is 25 times the lung ventilation.
Dead cavity
Anatomical dead space: The airway between the respiratory bronchi from the nasal passage cannot carry out gas exchange, and its air volume is about 150 ml.
Alveolar dead space: Even if gas enters the alveoli, gas exchange may not occur due to insufficient blood flow around the alveoli. This alveolar volume is the alveolar dead space. Normal supine position is close to zero.
Anatomical dead space Alveolar dead space = physiological dead space.
alveolar ventilation
Fresh air inhaled into the alveoli per minute = (tidal volume – dead space volume) × respiratory rate.
Normal (500-150)×12=4.2L/min
From the perspective of ventilation efficiency, deep and slow breathing is more efficient than shallow and fast breathing, but it will also increase the work of breathing.
Breathing work
The work done by the respiratory muscles to overcome the elastic resistance and inelastic resistance of the lungs and thorax to achieve pulmonary ventilation is usually expressed as the change in transmural pressure during a breath multiplied by the change in lung volume.
Overcoming elastic resistance accounts for 2/3.
Overcoming inelastic resistance accounts for 1/3.
Generally only accounts for 3-5% of the total body energy consumption.
Lung ventilation and tissue ventilation
Principle of ventilation: gas diffusion
Gas diffusion rate D∝△P·T·A·S/d·√MW
Gas partial pressure, etc. = total pressure of mixed gas × volume percentage occupied by the gas.
Diffusion rate: S/√MW, which is the characteristic of the gas itself. CO₂ is approximately 21.05 times that of O₂.
lung ventilation
subtopic
Definition: Pulmonary ventilation refers to the gas exchange process between the alveoli and pulmonary capillary blood.
Influencing factors
Physical factors: partial pressure difference, solubility, temperature, etc. The gas partial pressure difference determines the direction of gas diffusion and affects temperature. Ventilation dysfunction can reduce the wind pressure difference and hinder ventilation.
Anatomic factors: respiratory membrane area and thickness. The normal area is 40 square meters, which can be increased to 70 square meters for exercise to enhance ventilation. Decreased area: pneumonia, atelectasis, pneumothorax, pulmonary embolism; increased thickness: pulmonary edema, pulmonary fibrosis, both of which hinder ventilation.
Physiological factors: ventilation-blood flow ratio (Va/Q)
Definition: The ratio of alveolar ventilation per minute to pulmonary blood flow per minute.
The normal value is 0.84. When standing, the apex of the lung is about 2.5 and the base of the lung is about 0.6.
The respiratory membrane is composed of six layers: the liquid layer of pulmonary surfactant, the alveolar epithelial cell layer, the epithelial basement membrane, the gap between the alveolar epithelium and the capillary membrane (stromal layer), the basement membrane of the capillaries, and the capillary endothelial cells. layer. The average total thickness is about 0.6 microns, and some parts are only 0.2 microns, so gas can easily diffuse through.
The gas diffusion rate is inversely proportional to the thickness of the respiratory membrane. The thicker the respiratory membrane, the less gas is exchanged per unit time.
The gas diffusion rate is proportional to the diffusion area.
lung diffusion capacity
Definition: The number of milliliters of gas that diffuses through the respiratory membrane per minute under the action of unit partial pressure difference (0.1333KPa, 1mmHg).
Dl=V/Pa-Pc
Pa represents the average partial pressure of the gas in the alveolar air.
Pc represents the average partial pressure of the gas within the pulmonary capillary blood.
V represents the amount of gas passing through the respiratory membrane per minute.
tissue ventilation
Definition: The mechanism and influencing factors of tissue ventilation are similar to those of lung ventilation. The difference is that gas exchange occurs between the superfluous medium, and the partial pressure difference between oxygen and carbon dioxide on both sides of the diffusion membrane changes with the intensity and intensity of intracellular oxidative metabolism. Tissue gland flow varies.
Transport of gases in the blood
oxygen transport
Physical dissolution: very little, 1.5%, depends on gas partial pressure and solubility.
Chemical bonding: 98.5%.
Hb (hemoglobin) O₂→ (lung, PO₂ high) ← (tissue, PO₂ low) HbO₂
Characteristics of the combination of oxygen and hemoglobin
Rapid, reversible, does not require enzyme catalysis, and is affected by oxygen partial pressure.
The combination of oxygen with the divalent iron ions in hemoglobin is oxygenation rather than oxidation, and the ferric ions lose the ability to bind oxygen.
One molecule of hemoglobin can bind up to four molecules of oxygen, and one gram of hemoglobin can bind 1.34 ml of oxygen.
Blood oxygen capacity: The maximum amount of oxygen that hemoglobin in 100 ml of blood can combine is related to the hemoglobin content in the blood. Normally 100 ml of blood contains 15 grams of hemoglobin combined with 20.1 ml of oxygen
Blood oxygen content: The amount of oxygen actually combined with hemoglobin in 100 ml of blood is related to the hemoglobin content and blood oxygen partial pressure.
Blood oxygen saturation: The percentage of blood oxygen content and blood oxygen capacity is related to the partial pressure of oxygen.
Cyanosis
The deoxygenated hemoglobin in the superficial vascular bed of the body exceeds 50 grams per liter, and the skin and mucous membranes turn blue.
It is a sign of tissue hypoxia, but cyanosis does not necessarily mean hypoxia, such as at plateau; hypoxia does not necessarily mean cyanosis, such as anemia.
Hemoglobin has two conformations, R (loose) type and T (tight) type.
oxygen dissociation curve
Definition: A curve describing the relationship between oxygen partial pressure and hemoglobin oxygen saturation, reflecting the binding and dissociation of oxygen and hemoglobin. The curve is S-shaped, which is related to the allosteric effect of hemoglobin.
curve stage.
Upper section: 60~100mmHg, flat. It represents the combination of O₂ in the lungs and increases the oxygen partial pressure, which does not help to increase the oxygen saturation. As long as the oxygen partial pressure is greater than 60mmHg, the oxygen saturation can be greater than 90% and 90% without severe hypoxia.
Middle section: 40~60mmHg, shaking. Represents the part of blood that releases oxygen in tissues. Arterial blood flows through the tissues and becomes venous blood after ventilation. The partial pressure of oxygen drops from 100 to 40mmHg. Blood oxygen release, because the curve becomes steeper, a large amount of oxygen can be released.
Lower section: 15~40mmHg, steeper. Represents blood releasing oxygen reserves in tissues. When cell metabolism is enhanced, the partial pressure of oxygen in cells decreases, and arterial blood flows through the tissues and becomes venous blood, which further decreases at the level of 40mmHg. Because the curve is steeper, the partial pressure of oxygen drops slightly at this point, which can cause a large amount of oxygen to be released.
The middle and lower sections of the curve also mean that in severe hypoxia, pulmonary ventilation is slightly improved, and the partial pressure of oxygen is increased, which can significantly increase oxygen saturation and improve hypoxic symptoms.
Factors affecting the oxygen dissociation curve.
When the oxygen dissociation curve shifts to the left, hemoglobin's affinity for oxygen increases, which is beneficial to the combination of hemoglobin and oxygen; when the oxygen dissociation curve shifts to the right, hemoglobin's affinity for oxygen decreases, which is beneficial to the release of oxygen from hemoglobin.
Effect of carbon dioxide, hydrogen ions or pH value.
The influence of carbon dioxide and hydrogen ions on the oxygen dissociation curve is called the Bohr effect.
The left shift of the curve in the lungs favors the combination of hemoglobin with oxygen.
Shifting the tissue curve to the right is beneficial to the release of tissue oxygen.
Effect of temperature.
When the temperature increases, the curve shifts to the right, and when the temperature decreases, the curve shifts to the left.
Tissue metabolism is strengthened, the temperature rises, the curve shifts to the right, and the release of oxygen is increased.
Under hypothermic anesthesia, hemoglobin's affinity for oxygen increases, oxygen release decreases, and tissue hypoxia is prone to occur.
Effects of 2,3-bisphosphoglycerate (2,3-DPG).
2,3-bisphosphoglycerate is a product of red blood cell glycolysis, and the rising curve of 2,3-bisphosphoglycerate shifts to the right. The 2,3-bisphosphoglycerate reduction curve shifts to the left.
Old blood glycolysis stops, 2,3-bisphosphoglycerate. As the decline curve shifts to the left, the affinity of red blood cells for oxygen increases and oxygen release decreases. Therefore, old blood has poor ability to transport and release oxygen.
transport of carbon dioxide
Physical dissolution: 5%.
chemical bonding
Bicarbonate: 88%
CO₂ H₂O (carbonic anhydrase →←H₂CO₃→←HCO₃- H₊)
Carbamate hemoglobin: 7%, accounts for 17.4% of carbon dioxide released from the lungs
HbNH₂O₂ H₊ CO₂ (in tissues →← (in lungs) HHbNHCOOH O₂)
Holden effect: The combination of oxygen and hemoglobin can promote the release of carbon dioxide in the blood.
Regulation of respiratory movements
Respiratory center and rhythm formation
spinal cord
C3∽6: innervates the diaphragm
T1∽L3: innervates intercostal muscles and abdominal muscles
pons
Respiratory adjustment center: Located in the upper part of the pons, it includes the medial parabrachial nucleus (PB nucleus) and the KF nucleus group, collectively called the PBKF nucleus group. It can inhibit the inspiratory center and promote the conversion of inhalation into exhalation, which is related to the conversion of breathing patterns.
Long suction center: In the past, it was believed that there was a long suction center in the middle and lower part of the pons. Strengthens the excitement of the inspiratory center, causing long inhalation; it cannot be confirmed yet.
Medulla oblongata
It is the site where the basic rhythm of breathing is generated: it is divided into dorsal respiratory group (DRG) and ventral respiratory group (VRG), which is composed of a large number of respiratory neurons.
Inspiratory, expiratory, transtemporal (inhale-exhale, exhale-inhale) neurons.
Dorsal group (ventrolateral part of the nucleus of the solitary tract)
Iα-cross-diaphragm motor neuron
Ⅰβ—Receives input from Ⅰα and pulmonary stretch receptors
Ventral group (nucleus ambiguus, nucleus ambiguus and Bautzinger complex)
Ⅰγ—auxiliary respiratory muscles of the ipsilateral throat
—Crossing intercostal, external and abdominal muscle motor neurons
Ⅰδ—interneurons that inhibit respiratory neurons in the dorsal group
higher brain
Respiratory movements are also affected by centers above the pons, such as the cerebral cortex, limbic system, hypothalamus, etc.
The cerebral cortex controls the movement of lower brainstem respiratory neurons through the corticospinal tract and cortical brainstem tract to ensure the completion of other important respiratory-related activities.
Breathing does not require conscious control and can proceed in an automatic rhythm. It is autonomous breathing and is controlled by the lower brainstem (pons and medulla oblongata) - the autonomous respiratory rhythm regulation system.
Breathing can also be controlled by consciousness. This is voluntary breathing, controlled by the cerebral cortex - the voluntary breathing regulation system.
Can form a conditioned reflex of breathing movements.
The descending pathways of the two respiratory regulation systems are separate, and the separation of spontaneous breathing and voluntary breathing can be seen clinically.
Suction cut-off mechanism.
nascent cell theory
neuron network theory
reflex regulation of breathing
chemoreceptive reflex
peripheral chemoreceptors
carotid body, aortic body
Effective stimulation: Arterial blood PO₂ decreases, PCO₂ increases, H₊ concentration increases, and circulating blood volume decreases
central chemoreceptor
superficial ventrolateral medulla
Effective stimulation: H₊ increases in cerebrospinal fluid and local tissue fluid. Physiological stimulation comes from CO₂ in the blood and is characterized by high sensitivity and long incubation period.
Effects of CO₂, O₂ and H₊ in blood on breathing.
CO₂
Carbon dioxide is the most important humoral factor regulating breathing under physiological conditions.
A certain level of carbon dioxide in the blood is important for maintaining normal excitability of the respiratory center.
The increase in carbon dioxide in the inhaled air can cause excitement of the respiratory center through central and peripheral chemoreceptors, and increase pulmonary ventilation. Central chemoreceptors play the main role (80%), but peripheral chemoreceptors take effect first.
Excessive carbon dioxide in the inhaled air can cause carbon dioxide retention in the body, causing headaches, vomiting, and coma. On the contrary, it can inhibit breathing, which is called carbon dioxide anesthesia.
Missing O₂
The body is not sensitive to hypoxic stimulation and will be excited to breathe only when the partial pressure of oxygen is less than 80mmHg.
During hypoxia, breathing can be stimulated through peripheral chemoreceptors.
The direct effect of hypoxia on the respiratory center is to inhibit it. Therefore, when there is severe hypoxia, the direct inhibitory effect of hypoxia on the respiratory center will exceed its indirect excitatory effect through peripheral chemoreceptors, causing respiratory depression instead.
Elevated H₊ in the blood
An increase in the concentration of hydrogen ions in the blood can cause excitement in the respiratory center through peripheral and central chemoreceptors. However, because hydrogen ions in the blood cannot easily pass through the blood-brain barrier, peripheral effects are dominant.
There can be interactions, synergies or offsets between the three.
pulmonary stretch reflex
Definition: An inspiratory depression or excitement reflex caused by lung enlargement or lung contraction.
Lung expansion reflex: Inspiratory depression.
Inhale → lung expansion → (bronchial and bronchiolar smooth muscles) stretch receptors ⊕ → vagus nerve → inhibit inspiratory center → terminate inhalation.
Significance: Convert inhalation to exhalation in time, which plays a role in maintaining breathing depth and breathing frequency; depending on species, this reflex has little effect in the human body.
Cutting off the vagus nerve lengthens and deepens the inhalation, slowing down the breathing rate.
Pulmonary contraction reflex: expiratory depression.
Meaning: To prevent exhaling too deeply.