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Pathophysiology - hypoxia
Hypoxia, a pathological process, not only affects the metabolism and function of the tissue, but also may trigger abnormal changes in morphological structure. From hypotonic hypoxia to oxygen poisoning, the body's reactions are complex and diverse. The central nervous system, circulatory system, respiratory system and other systems show different compensation and damage when hypoxia. Although oxygen therapy is best for hypotonic hypoxia, oxygen exceeding 05 atmospheres may cause oxygen poisoning. Factors such as age, cardiopulmonary health, and body temperature significantly affect the body's tolerance to hypoxia. Understanding these mechanisms will help us better address the challenges posed by hypoxia.
Edited at 2025-03-10 15:36:18- Rumi 10 spiritual high-dimensional awakenings
Rumi: 10 dimensions of spiritual awakening. When you stop looking for yourself, you will find the entire universe because what you are looking for is also looking for you. Anything you do persevere every day can open a door to the depths of your spirit. In silence, I slipped into the secret realm, and I enjoyed everything to observe the magic around me, and didn't make any noise. Why do you like to crawl when you are born with wings? The soul has its own ears and can hear things that the mind cannot understand. Seek inward for the answer to everything, everything in the universe is in you. Lovers do not end up meeting somewhere, and there is no parting in this world. A wound is where light enters your heart.
- Pathophysiology - Heart failure
Chronic heart failure is not just a problem of the speed of heart rate! It is caused by the decrease in myocardial contraction and diastolic function, which leads to insufficient cardiac output, which in turn causes congestion in the pulmonary circulation and congestion in the systemic circulation. From causes, inducement to compensation mechanisms, the pathophysiological processes of heart failure are complex and diverse. By controlling edema, reducing the heart's front and afterload, improving cardiac comfort function, and preventing and treating basic causes, we can effectively respond to this challenge. Only by understanding the mechanisms and clinical manifestations of heart failure and mastering prevention and treatment strategies can we better protect heart health.
- Pathophysiology - ischemia - reperfusion injury
Ischemia-reperfusion injury is a phenomenon that cellular function and metabolic disorders and structural damage will worsen after organs or tissues restore blood supply. Its main mechanisms include increased free radical generation, calcium overload, and the role of microvascular and leukocytes. The heart and brain are common damaged organs, manifested as changes in myocardial metabolism and ultrastructural changes, decreased cardiac function, etc. Prevention and control measures include removing free radicals, reducing calcium overload, improving metabolism and controlling reperfusion conditions, such as low sodium, low temperature, low pressure, etc. Understanding these mechanisms can help develop effective treatment options and alleviate ischemic injury.
Pathophysiology - hypoxia
- Rumi 10 spiritual high-dimensional awakenings
Rumi: 10 dimensions of spiritual awakening. When you stop looking for yourself, you will find the entire universe because what you are looking for is also looking for you. Anything you do persevere every day can open a door to the depths of your spirit. In silence, I slipped into the secret realm, and I enjoyed everything to observe the magic around me, and didn't make any noise. Why do you like to crawl when you are born with wings? The soul has its own ears and can hear things that the mind cannot understand. Seek inward for the answer to everything, everything in the universe is in you. Lovers do not end up meeting somewhere, and there is no parting in this world. A wound is where light enters your heart.
- Pathophysiology - Heart failure
Chronic heart failure is not just a problem of the speed of heart rate! It is caused by the decrease in myocardial contraction and diastolic function, which leads to insufficient cardiac output, which in turn causes congestion in the pulmonary circulation and congestion in the systemic circulation. From causes, inducement to compensation mechanisms, the pathophysiological processes of heart failure are complex and diverse. By controlling edema, reducing the heart's front and afterload, improving cardiac comfort function, and preventing and treating basic causes, we can effectively respond to this challenge. Only by understanding the mechanisms and clinical manifestations of heart failure and mastering prevention and treatment strategies can we better protect heart health.
- Pathophysiology - ischemia - reperfusion injury
Ischemia-reperfusion injury is a phenomenon that cellular function and metabolic disorders and structural damage will worsen after organs or tissues restore blood supply. Its main mechanisms include increased free radical generation, calcium overload, and the role of microvascular and leukocytes. The heart and brain are common damaged organs, manifested as changes in myocardial metabolism and ultrastructural changes, decreased cardiac function, etc. Prevention and control measures include removing free radicals, reducing calcium overload, improving metabolism and controlling reperfusion conditions, such as low sodium, low temperature, low pressure, etc. Understanding these mechanisms can help develop effective treatment options and alleviate ischemic injury.
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Section 1. Introduction
concept
When the tissue cannot obtain oxygen or cannot make full use of oxygen, the metabolism, function, and even morphological structure of the tissue may undergo abnormal changes, and this pathological process becomes hypoxia.
The oxygen stored in the body is only 1.5L, but it requires about 250ml of aerobic acid per minute.
The brain and heart have high demand for oxygen
Blood oxygen index
Oxygen partial pressure PO2
Refers to the tension generated by oxygen dissolved in the blood
Arterial blood oxygen partial pressure PaO2
Normal value
100mmHg
13.3KPa
Factors
Mainly the partial pressure of oxygen inhaled gas
e.g.Plateau area
Functional status of the lungs
e.g. Cannot allow oxygen to fully enter the body
＞60mmHg is not hypoxia
No significant change in blood oxygen saturation at above 60 (oxygen separation curve)
Venous blood oxygen partial pressure PvO2
Normal value
40mmHg
5.33KPa
Oxygen capacity CO2max
Concept: refers to the maximum oxygen carrying amount when Hb in the blood is fully saturated.
depending on
The quality of Hb
The amount of Hb
CO2max=1.34 (ml/g)×Hb(g/dl)≈20ml/dl
It is an ideal state and cannot be achieved. Reflects the ability of a person to carry oxygen
Oxygen content CO2
Concept: refers to the actual oxygen carrying amount of 100ml of blood
The actual oxygen bound to Hb
Very small amount of oxygen dissolved in plasma (about 0.3 ml/dl)
It depends mainly on
Partial oxygen pressure
Within a certain range, as PO2 increases, the oxygen content increases
Oxygen capacity
Normal value
Arterial blood oxygen content CaO2
19ml/dl
Venous blood oxygen content CvO2
14ml/dl
Arteriovenous oxygen content difference = 5ml/dl
Oxygen saturation SO2
Concept: refers to the oxygen saturation of Hb
SO2=[(oxygen content-dissolved oxygen)/oxygen capacity]×100%
Factors
Depends on the partial oxygen pressure
In addition, 2, 3-DPG↑, acidosis, blood CO2↑, blood temperature↑→Reduce the affinity of Hb and O2→SO2↓
Normal value
Arterial oxygen saturation SaO2
95%
Sensitive, strict
Arterial blood oxygen saturation SvO2
70%
P50
Concept: refers to the partial oxygen pressure when the Hb oxygen saturation is 50%.
Normal value: 26-27mmHg (3.47-3.6KP)
Reflects the affinity of Hb and O2
P50 increases → decreases affinity
Section 2. Types of hypoxia
Oxygen Utilization
External breathing
Lung ventilation
Lung ventilation
Transport of gas
The quality and quantity of Hb
Blood circulation
Inner breathing
Mitochondrial oxidative phosphorylation disorder
Types of hypoxia
Hypotonic hypoxia
reason
The partial pressure of oxygen inhaled gas is too low
PaO2 is mainly affected by partial pressure of oxygen inhaled gas
e.g. Plateau areas, abandoned mines
External respiratory dysfunction
e.g. Airway obstruction, pulmonary edema, etc.
Most common in clinical practice
Venous blood flow artery
Commonly found in congenital heart disease, especially ventricular septal defect
Blood oxygen changes
PaO2↓, CaO2↓, SaO2↓, CaO2-CvO2↓ (low oxygen partial pressure → oxygen dispersion velocity ↓→ tissue hypoxia)
CO2max is normal
The quality and quantity of Hb are normal
Notice
When PaO2 is <60mmHg, CaO2 and SaO2 will be significantly reduced
There is cyanosis
Concept: refers to the phenomenon that the deoxygenated Hb concentration in cap. increases to more than 5g/dl, and the skin and mucous membranes appear in purple.
Normally, the deoxygenated Hb concentration in cap. is about 2.6g/dl
e.g. Infants and young children cry for a long time
Blood hypoxia
Concept: refers to tissue hypoxia caused by the decrease in the amount of Hb or the change in properties, resulting in a decrease in blood oxygen content or the difficulty of release of Hb-bound O2.
reason
anemia
Iron deficiency anemia, hemolytic anemia
CO poisoning
CO and Hb are not easy to bind to peptides (carbon-oxygen Hb), but it is difficult to separate → CO and Hb affinity is much higher than the binding force of O2 and Hb
Carbonoxyhemoglobin can also inhibit the release of O2 by oxygenated Hb
Metallurglobinemia
Most of the normal Hb ions are Fe2, but in some pathological conditions, more Fe3 appears
Fe3 cannot bind O2 and can inhibit the release of O2 by normal oxygenation Hb.
Intestinal cyanosis
Patients eat a large amount of nitrate (pickled vegetables), which is reduced to nitrite (strong oxidant) by bacteria in the intestines, which can lead to high-iron Hb blood
"Cyanosis" is commonly known as "Cyanosis"
Abnormal enhancement of Hb and oxygen
e.g. The oxygen separation curve shifts left during alkaline poisoning
O2 cannot be fully released from venous blood
Blood oxygen changes
PaO2 is normal → SaO2 is normal or ↑
CO2max↓ or normal, CO2↓ or ↑
CaO2-CvO2↓
Features
No cyanosis
Cause: Deoxygenated Hb cannot reach 5g/dl
Anemia: pale face
CO poisoning: The skin and mucous membranes appear cherry-red
Metallurglobinemia: brown or bluestone slab color of skin and mucous membranes
Circulating hypoxia
Concept: Reduced blood flow in tissue reduces oxygen supply in tissues, which are divided into
Ischemic hypoxia
Blood-congestive hypoxia
reason
Systemic sex
shock
Heart failure
Locality
embolism
Vascular lesions
Blood oxygen changes
PaO2 is normal, CaO2max is normal, CaO2 is normal, SaO2 is normal
CaO2-CvO2↑
Blood flow velocity↓→The amount of oxygen obtained by tissue cells from unit blood↑
Time factor must be considered
Deoxygenation Hb↑→Cyanosis at the cap.
Tissue hypoxia
Concept: refers to hypoxia caused by the use of oxygen disorders in histocellular cells
reason
Tissue Poisoning: Cyanide (blocking the respiratory chain), sulfide
Cell damage: radiation, bacterial, etc.
Respiratory enzyme synthesis disorder
Blood oxygen changes
PaO2 is normal, CaO2max is normal, CaO2 is normal, SaO2 is normal
CaO2-CvO2↓
No cyanosis
Section 3. Changes in the timing of hypotonic hypoxia
Respiratory system
Compensation reaction
condition:
PaO2＜60mmHg/8KPa
PaO2↓→Peripheral chemoreceptors (carotid and aortic bodies)→Central →Pulmonary ventilation↑ (most important for acute hypoxia)
e.g. Altitude reaction: At the same time, it will lead to respiratory alkalosis, inhibit ventilation → the amount of ventilation will not increase significantly at the beginning; after 3-4 days, due to the onset of kidney compensation → ventilation will increase significantly
damage
Pulmonary edema
It is manifested as dyspnea, cough, bloody foaming sputum, cyanosis of the skin and mucous membranes, etc.
Mechanism: Cap. Increased internal pressure and enhanced permeability can cause fluid to penetrate into the alveoli and bronchial, causing external respiratory disorders
Circulation system
Compensation reaction
Increased cardiac output
Accelerate heart rate
Increased lung ventilation → stimulated lung stretch receptors → caused sympathetic N excitation → heart rate ↑
Increased myocardial contractility
It's also related to sympathetic excitement
Increased venous return
Increased lung ventilation to increase the chest pressure/increased cardiac action → help venous return
Blood flow redistribution
change
Relatively increased cardiovascular and cerebrovascular blood flow
Reduced blood flow to the skin, mucous membranes and internal organs
mechanism
Hypoxia stress → Sympathetic N excitation, release of catecholamines → mainly contract blood vessels through α1R
But there are fewer α1 receptors in the cardiovascular and cerebrovascular system
Anaerobic metabolites (lactic acid, adenosine, histamine, etc.) in hypoxia → vascular expansion → cardiovascular and cerebrovascular blood supply↑
Pulmonary vascular contraction
Significance: Maintain the ventilation and blood flow ratio of the alveoli. Under normal circumstances:
Ventilation↓→The blood flow through cannot be arterialized
Blood flow↓→Create ineffective ventilation
mechanism
The role of sympathetic N
The role of bodily fluid factors
Vascular shrinkage substances: thrombin A2 (TXA2), endothelin (ET)
Vascular dilated substances: prostacyclin (PGT2), NO
Shrinkage or expansion depends on the dominant substance
The direct effect of hypoxia on vascular smooth muscle
Involves ion channel changes
Contractive reaction of smooth muscle
cap.
Make the cap. closer contact with tissue cells
For chronic hypoxia (COPD, etc.), the others are only for acute hypoxia
damage
Decreased contraction and diastolic function of myocardium
Arrhythmia, bradycardia, pre-systolic ventricular tremor
Pulmonary hypertension
Reduced venous return
Severe hypoxia → respiratory center depression
Blood system
Compensation reaction
Red blood cells
mechanism
Mainly, tubular interstitial cells and other renal tubular cells feel hypoxia → secrete erythropoietin EPO↑
EPO promotes bone marrow hematopoiesis
The final oxygen capacity and oxygen content are all ↑
2, 3-DPG↑, make Hb and O2 affinity↓
Results: The oxygen separation curve moves right, making it easier to release oxygen
Conditions: PO2 is maintained above 60mmHg → Ensure that enough Hb is combined with O2
mechanism
2.3-DPG can be combined with deoxygenated Hb, making its configuration stable and not easy to bind to O2.
2,3-DPG is an acid that reduces its affinity through the Bohr effect
Compensation is basically aimed at chronic hypoxia and is basically beneficial
Central nervous system
symptom
Acute hypoxia
Significant symptoms: mild headache, emotional excitement, decreased thinking, memory, judgment, etc., and inconsistent exercise
Chronic hypoxia
Fatigue, lethargy, depression, etc.
Complex mechanism
Cell membrane potential ↓, neuromedia synthesis ↓, ATP ↓, acidosis, intracellular Ca2 overload, lysosomal destruction, etc.
Tissue cells
Compensation reaction
The ability of cells to use oxygen↑
Mechanism - mainly mitochondrial
Quantity ↑
Endometrium area↑
Number and activity of oxidative phosphorylation-related enzymes in a small amount of hypoxia↑
For chronic hypoxia
Acute hypoxia-reduced arteriovenous oxygen content
Chronic hypoxia - Through compensation, the difference in arteriovenous oxygen content remains normal range
Anaerobic fermentation↑
Ensure ATP supply
Myoglobin↑
Can store more O2 for immediate needs
Low metabolic state
Reduce the need for energy, etc., and reduce the damage to cells by hypoxia
damage
Mainly - cell membrane
change
Na Inflow
Causes cell swelling
K Outflow
Influence intracellular anabolic
Ca2 Inflow
Ca overload → activate phospholipase → destroy membrane; increase in cell free radicals; destroy mitochondria, etc.
Mechanism: The main reason is that the ion pump activity is weakened, which is not enough to combat ion flow caused by the difference in concentration
Mitochondria
Mild hypoxia can enhance its function. When hypoxia is severe, enzyme activity may even collapse.
Lysosomes
The e.g. membrane is destroyed, and the enzyme is released to destroy the cell itself
Section 4. Factors affecting the body's tolerance to hypoxia
Metabolic oxygen consumption rate
Low tolerance to hypoxia during fever and hyperthyroidism
High tolerance to hypoxia when body temperature is reduced and nervous system inhibits
Clinical "hypothermia" is performed to reduce the damage of ischemia and hypoxia to the heart, etc.
The body's metabolic capacity
Age, cardiopulmonary health, etc.
Section 5. Oxygen therapy and oxygen poisoning
Oxygen therapy
The best effect on hypotonic hypoxia
For other types of hypoxia
Oxygen therapy has limited effect
High pressure oxygen—can increase physically dissolved oxygen in plasma
e.g. Treatment of patients with CO poisoning
Oxygen poisoning
Oxygen above 0.5 atmospheres has a toxic effect on cells and may cause oxygen poisoning
Emphasize the partial pressure of oxygen, not the concentration of oxygen
mechanism
Probably related to reactive oxygen species
Clinical manifestations
Pulmonary oxygen poisoning
Inhaling O2 at an atmospheric pressure for about 8 hours
Respiratory disorders
Cough, dyspnea, blood type foam phlegm, etc.
Brain oxygen poisoning
It appears after inhaling 2-3 atmospheric pressure O2 for a few hours
Central nervous system disorders
Audiovisual disorders, nausea, convulsions, coma, etc.
Deficiency of oxygen
Section 1. Introduction
concept
When the tissue cannot obtain oxygen or cannot make full use of oxygen, the metabolism, function, and even morphological structure of the tissue may undergo abnormal changes, and this pathological process becomes hypoxia.
The oxygen stored in the body is only 1.5L, but it requires about 250ml of aerobic acid per minute.
The brain and heart have high demand for oxygen
Blood oxygen index
Oxygen partial pressure PO2
Refers to the tension generated by oxygen dissolved in the blood
Arterial blood oxygen partial pressure PaO2
Normal value
100mmHg
13.3KPa
Factors
Mainly the partial pressure of oxygen inhaled gas
e.g.Plateau area
Functional status of the lungs
e.g. Cannot allow oxygen to fully enter the body
＞60mmHg is not hypoxia
No significant change in blood oxygen saturation at above 60 (oxygen separation curve)
Venous blood oxygen partial pressure PvO2
Normal value
40mmHg
5.33KPa
Oxygen capacity CO2max
Concept: refers to the maximum oxygen carrying amount when Hb in the blood is fully saturated.
depending on
The quality of Hb
The amount of Hb
CO2max=1.34 (ml/g)×Hb(g/dl)≈20ml/dl
It is an ideal state and cannot be achieved. Reflects the ability of a person to carry oxygen
Oxygen content CO2
Concept: refers to the actual oxygen carrying amount of 100ml of blood
The actual oxygen bound to Hb
Very small amount of oxygen dissolved in plasma (about 0.3 ml/dl)
It depends mainly on
Partial oxygen pressure
Within a certain range, as PO2 increases, the oxygen content increases
Oxygen capacity
Normal value
Arterial blood oxygen content CaO2
19ml/dl
Venous blood oxygen content CvO2
14ml/dl
Arteriovenous oxygen content difference = 5ml/dl
Oxygen saturation SO2
Concept: refers to the oxygen saturation of Hb
SO2=[(oxygen content-dissolved oxygen)/oxygen capacity]×100%
Factors
Depends on the partial oxygen pressure
In addition, 2, 3-DPG↑, acidosis, blood CO2↑, blood temperature↑→Reduce the affinity of Hb and O2→SO2↓
Normal value
Arterial oxygen saturation SaO2
95%
Sensitive, strict
Arterial blood oxygen saturation SvO2
70%
P50
Concept: refers to the partial oxygen pressure when the Hb oxygen saturation is 50%.
Normal value: 26-27mmHg (3.47-3.6KP)
Reflects the affinity of Hb and O2
P50 increases → decreases affinity
Section 2. Types of hypoxia
Oxygen Utilization
External breathing
Lung ventilation
Lung ventilation
Transport of gas
The quality and quantity of Hb
Blood circulation
Inner breathing
Mitochondrial oxidative phosphorylation disorder
Types of hypoxia
Hypotonic hypoxia
reason
The partial pressure of oxygen inhaled gas is too low
PaO2 is mainly affected by partial pressure of oxygen inhaled gas
e.g. Plateau areas, abandoned mines
External respiratory dysfunction
e.g. Airway obstruction, pulmonary edema, etc.
Most common in clinical practice
Venous blood flow artery
Commonly found in congenital heart disease, especially ventricular septal defect
Blood oxygen changes
PaO2↓, CaO2↓, SaO2↓, CaO2-CvO2↓ (low oxygen partial pressure → oxygen dispersion velocity ↓→ tissue hypoxia)
CO2max is normal
The quality and quantity of Hb are normal
Notice
When PaO2 is <60mmHg, CaO2 and SaO2 will be significantly reduced
There is cyanosis
Concept: refers to the phenomenon that the deoxygenated Hb concentration in cap. increases to more than 5g/dl, and the skin and mucous membranes appear in purple.
Normally, the deoxygenated Hb concentration in cap. is about 2.6g/dl
e.g. Infants and young children cry for a long time
Blood hypoxia
Concept: refers to tissue hypoxia caused by the decrease in the amount of Hb or the change in properties, resulting in a decrease in blood oxygen content or the difficulty of release of Hb-bound O2.
reason
anemia
Iron deficiency anemia, hemolytic anemia
CO poisoning
CO and Hb are not easy to bind to peptides (carbon-oxygen Hb), but it is difficult to separate → CO and Hb affinity is much higher than the binding force of O2 and Hb
Carbonoxyhemoglobin can also inhibit the release of O2 by oxygenated Hb
Metallurglobinemia
Most of the normal Hb ions are Fe2, but in some pathological conditions, more Fe3 appears
Fe3 cannot bind O2 and can inhibit the release of O2 by normal oxygenation Hb.
Intestinal cyanosis
Patients eat a large amount of nitrate (pickled vegetables), which is reduced to nitrite (strong oxidant) by bacteria in the intestines, which can lead to high-iron Hb blood
"Cyanosis" is commonly known as "Cyanosis"
Abnormal enhancement of Hb and oxygen
e.g. The oxygen separation curve shifts left during alkaline poisoning
O2 cannot be fully released from venous blood
Blood oxygen changes
PaO2 is normal → SaO2 is normal or ↑
CO2max↓ or normal, CO2↓ or ↑
CaO2-CvO2↓
Features
No cyanosis
Cause: Deoxygenated Hb cannot reach 5g/dl
Anemia: pale face
CO poisoning: The skin and mucous membranes appear cherry-red
Metallurglobinemia: brown or bluestone slab color of skin and mucous membranes
Circulating hypoxia
Concept: Reduced blood flow in tissue reduces oxygen supply in tissues, which are divided into
Ischemic hypoxia
Blood-congestive hypoxia
reason
Systemic sex
shock
Heart failure
Locality
embolism
Vascular lesions
Blood oxygen changes
PaO2 is normal, CaO2max is normal, CaO2 is normal, SaO2 is normal
CaO2-CvO2↑
Blood flow velocity↓→The amount of oxygen obtained by tissue cells from unit blood↑
Time factor must be considered
Deoxygenation Hb↑→Cyanosis at the cap.
Tissue hypoxia
Concept: refers to hypoxia caused by the use of oxygen disorders in histocellular cells
reason
Tissue Poisoning: Cyanide (blocking the respiratory chain), sulfide
Cell damage: radiation, bacterial, etc.
Respiratory enzyme synthesis disorder
Blood oxygen changes
PaO2 is normal, CaO2max is normal, CaO2 is normal, SaO2 is normal
CaO2-CvO2↓
No cyanosis
Section 4. Factors affecting the body's tolerance to hypoxia
Metabolic oxygen consumption rate
Low tolerance to hypoxia during fever and hyperthyroidism
High tolerance to hypoxia when body temperature is reduced and nervous system inhibits
Clinical "hypothermia" is performed to reduce the damage of ischemia and hypoxia to the heart, etc.
The body's metabolic capacity
Age, cardiopulmonary health, etc.
Section 5. Oxygen therapy and oxygen poisoning
Oxygen therapy
The best effect on hypotonic hypoxia
For other types of hypoxia
Oxygen therapy has limited effect
High pressure oxygen—can increase physically dissolved oxygen in plasma
e.g. Treatment of patients with CO poisoning
Oxygen poisoning
Oxygen above 0.5 atmospheres has a toxic effect on cells and may cause oxygen poisoning
Emphasize the partial pressure of oxygen, not the concentration of oxygen
mechanism
Probably related to reactive oxygen species
Clinical manifestations
Pulmonary oxygen poisoning
Inhaling O2 at an atmospheric pressure for about 8 hours
Respiratory disorders
Cough, dyspnea, blood type foam phlegm, etc.
Brain oxygen poisoning
It appears after inhaling 2-3 atmospheric pressure O2 for a few hours
Central nervous system disorders
Audiovisual disorders, nausea, convulsions, coma, etc.
Section 3. Changes in the timing of hypotonic hypoxia
Respiratory system
Compensation reaction
condition:
PaO2＜60mmHg/8KPa
PaO2↓→Peripheral chemoreceptors (carotid and aortic bodies)→Central →Pulmonary ventilation↑ (most important for acute hypoxia)
e.g. Altitude reaction: At the same time, it will lead to respiratory alkalosis, inhibit ventilation → the amount of ventilation will not increase significantly at the beginning; after 3-4 days, due to the onset of kidney compensation → ventilation will increase significantly
damage
Pulmonary edema
It is manifested as dyspnea, cough, bloody foaming sputum, cyanosis of the skin and mucous membranes, etc.
Mechanism: Cap. Increased internal pressure and enhanced permeability can cause fluid to penetrate into the alveoli and bronchial, causing external respiratory disorders
Circulation system
Compensation reaction
Increased cardiac output
Accelerate heart rate
Increased lung ventilation → stimulated lung stretch receptors → caused sympathetic N excitation → heart rate ↑
Increased myocardial contractility
It's also related to sympathetic excitement
Increased venous return
Increased lung ventilation to increase the chest pressure/increased cardiac action → help venous return
Blood flow redistribution
change
Relatively increased cardiovascular and cerebrovascular blood flow
Reduced blood flow to the skin, mucous membranes and internal organs
mechanism
Hypoxia stress → Sympathetic N excitation, release of catecholamines → mainly contract blood vessels through α1R
But there are fewer α1 receptors in the cardiovascular and cerebrovascular system
Anaerobic metabolites (lactic acid, adenosine, histamine, etc.) in hypoxia → vascular expansion → cardiovascular and cerebrovascular blood supply↑
Pulmonary vascular contraction
Significance: Maintain the ventilation and blood flow ratio of the alveoli. Under normal circumstances:
Ventilation↓→The blood flow through cannot be arterialized
Blood flow↓→Create ineffective ventilation
mechanism
The role of sympathetic N
The role of bodily fluid factors
Vascular shrinkage substances: thrombin A2 (TXA2), endothelin (ET)
Vascular dilated substances: prostacyclin (PGT2), NO
Shrinkage or expansion depends on the dominant substance
The direct effect of hypoxia on vascular smooth muscle
Involves ion channel changes
Contractive reaction of smooth muscle
cap.
Make the cap. closer contact with tissue cells
For chronic hypoxia (COPD, etc.), the others are only for acute hypoxia
damage
Decreased contraction and diastolic function of myocardium
Arrhythmia, bradycardia, pre-systolic ventricular tremor
Pulmonary hypertension
Reduced venous return
Severe hypoxia → respiratory center depression
Blood system
Compensation reaction
Red blood cells
mechanism
Mainly, tubular interstitial cells and other renal tubular cells feel hypoxia → secrete erythropoietin EPO↑
EPO promotes bone marrow hematopoiesis
The final oxygen capacity and oxygen content are all ↑
2, 3-DPG↑, make Hb and O2 affinity↓
Results: The oxygen separation curve moves right, making it easier to release oxygen
Conditions: PO2 is maintained above 60mmHg → Ensure that enough Hb is combined with O2
mechanism
2.3-DPG can be combined with deoxygenated Hb, making its configuration stable and not easy to bind to O2.
2,3-DPG is an acid that reduces its affinity through the Bohr effect
Compensation is basically aimed at chronic hypoxia and is basically beneficial
Central nervous system
symptom
Acute hypoxia
Significant symptoms: mild headache, emotional excitement, decreased thinking, memory, judgment, etc., and inconsistent exercise
Chronic hypoxia
Fatigue, lethargy, depression, etc.
Complex mechanism
Cell membrane potential ↓, neuromedia synthesis ↓, ATP ↓, acidosis, intracellular Ca2 overload, lysosomal destruction, etc.
Tissue cells
Compensation reaction
The ability of cells to use oxygen↑
Mechanism - mainly mitochondrial
Quantity ↑
Endometrium area↑
Number and activity of oxidative phosphorylation-related enzymes in a small amount of hypoxia↑
For chronic hypoxia
Acute hypoxia-reduced arteriovenous oxygen content
Chronic hypoxia - Through compensation, the difference in arteriovenous oxygen content remains normal range
Anaerobic fermentation↑
Ensure ATP supply
Myoglobin↑
Can store more O2 for immediate needs
Low metabolic state
Reduce the need for energy, etc., and reduce the damage to cells by hypoxia
damage
Mainly - cell membrane
change
Na Inflow
Causes cell swelling
K Outflow
Influence intracellular anabolic
Ca2 Inflow
Ca overload → activate phospholipase → destroy membrane; increase in cell free radicals; destroy mitochondria, etc.
Mechanism: The main reason is that the ion pump activity is weakened, which is not enough to combat ion flow caused by the difference in concentration
Mitochondria
Mild hypoxia can enhance its function. When hypoxia is severe, enzyme activity may even collapse.
Lysosomes
The e.g. membrane is destroyed, and the enzyme is released to destroy the cell itself