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Pathophysiology - Acid-base balance disorder
Do you know that the diagnosis and treatment of acid-base balance disorders are much more complicated than imagined? Acid-base balance disorders are divided into simple and mixed, including metabolic acidosis and respiratory alkalosis. Indicators such as pH, PaCO2, bicarbonate, etc. are the key to diagnosis, but sometimes it is difficult to distinguish between respiratory or metabolic disorders. Acute respiratory acidosis is usually decompensated, the pH may be normal, and it is difficult to determine. Mixed acid-base balance disorders such as acid-base-based acupuncture and alkali-based acupuncture are more challenging to treat. Understanding the source, homeostasis and compensation regulation mechanism of acid and alkali substances is crucial for prevention and treatment. Only by mastering this knowledge can we better deal with complex acid-base balance disorders.
Edited at 2025-03-10 15:35:42- 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 - Acid-base balance disorder
- 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.
- Recommended to you
- Outline
Section 1. Source and steady state of acid and alkali substances
source
acid
Volatile acids - can be excreted through the lungs
Carbonated acid
Fixed acid - mainly excreted through the kidneys
Other acids besides carbonic acid. Sulfuric acid, phosphoric acid, lactic acid, pyruvate, etc.
Alkali
Mainly produced by in vivo metabolism
Vegetables, fruits
Adjustment of acid and base balance
Buffering effect of blood
The buffer pair consists of weak acids and their corresponding bases
e.g.
H2CO3—HCO3-
The strongest buffering capability
Cannot buffer carbonic acidosis/respiratory acidosis
HHb—Hb-
...
The regulatory effect of the lungs
Regulate CO2 emission
mechanism
PCO2↑/H ↑ → central/peripheral chemoreceptors → respiratory center excitation → lung ventilation ↑ → CO2 excretion ↑
The regulatory effect of the kidney
Proximal tubules
Hydrogen secretion → alkali preservation
Implemented through H-Na exchange
H secreted into the lumen → generate carbonic acid with HCO3 → generate CO2 under the action of carbonic anhydrase → return to blood → HCO3-absorbing
H -ATPase
Only H row
Distal tubules
H -ATPase/Proton Pump
Secrete NH3
e.g. Acidosis →NH3 formation increases → Combined with H to produce NH4 and excrete it out of the body
H-K exchange between tissue cells
See "Potassium Ion Disorder"
Hyperkalemia ↔ acidosis
Hypokalemia ↔alkalosis
Acid-base balance disorder
Section 1. Source and steady state of acid and alkali substances
source
acid
Volatile acids - can be excreted through the lungs
Carbonated acid
Fixed acid - mainly excreted through the kidneys
Other acids besides carbonic acid. Sulfuric acid, phosphoric acid, lactic acid, pyruvate, etc.
Alkali
Mainly produced by in vivo metabolism
Vegetables, fruits
Adjustment of acid and base balance
Buffering effect of blood
The buffer pair consists of weak acids and their corresponding bases
e.g.
H2CO3—HCO3-
The strongest buffering capability
Cannot buffer carbonic acidosis/respiratory acidosis
HHb—Hb-
...
The regulatory effect of the lungs
Regulate CO2 emission
mechanism
PCO2↑/H ↑ → central/peripheral chemoreceptors → respiratory center excitation → lung ventilation ↑ → CO2 excretion ↑
The regulatory effect of the kidney
Proximal tubules
Hydrogen secretion → alkali preservation
Implemented through H-Na exchange
H secreted into the lumen → generate carbonic acid with HCO3 → generate CO2 under the action of carbonic anhydrase → return to blood → HCO3-absorbing
H -ATPase
Only H row
Distal tubules
H -ATPase/Proton Pump
Secrete NH3
e.g. Acidosis →NH3 formation increases → Combined with H to produce NH4 and excrete it out of the body
H-K exchange between tissue cells
See "Potassium Ion Disorder"
Hyperkalemia ↔ acidosis
Hypokalemia ↔alkalosis
Section 2. Commonly used acid and alkali indicators
PH value
Normal 7.35-7.45
＞7.45→Alkalacterial poisoning
＜7.35→Acidtoxicity
Can't tell whether it's respiratory or metabolic
PaCO2 (partial pressure of arterial blood CO2)
Normal 33-46mmHg
＞46mmHg
Respiratory acidosis
Metabolic alkalosis after compensation
＜33mmHg
Respiratory alkalosis
Metabolic acidosis after compensation
Bicarbonate
Standard bicarbonate SB
HCO3-concentration measured in whole blood under standard conditions
Normal: 22-27mmol/L
Metabolic acidosis SB < 22mmol/L
Metabolic alkalosis SB>27mmol/L
Actual bicarbonate AB
The HCO3-concentration measured by blood samples isolated from air under actual conditions
AB=SB in normal people (the average CO2 partial pressure in normal people is 40mmHg)
Same problem as PH indicator reaction - it is impossible to tell whether it is respiratory or metabolic
AB＞SB
CO2 partial pressure in the body↑→Respiratory acidosis, metabolic alkalosis after compensation
AB＜SB
CO2 partial pressure in the body↓→Respiratory alkalosis, metabolic acidosis after compensation
Buffer alkali BB
The sum of all negative ions in the blood that have buffering capacity
Normal value: 45-51mmol/L
BB Changes
Metabolic acidosis →BB↓
Metabolic alkalosis →BB↑
Alkali remaining BE
Refers to the acid or alkali concentration required for titration of whole blood specimens with acid or alkali under standard conditions (same as SB) when pH=7.40
Normal value: -3— 3mmol/L
Acid titration → alkali residue → BE
Need for alkali titration → alkali deletion →-BE
BE changes
Metabolic acidosis
Negative value increases
Metabolic alkalosis
Positive value increases
Anion gap AG
Refers to the difference between the undetermined anion UA and the undetermined cation UC in plasma
UA
Some relatively unfixed anions
UC
Certain cations with relatively unfixed normal content
AG=UA-UC
calculate
UA Determinable Anion = UC Determinable Cation
→UA-UC=determinable cation-determinable anion
→AG=Na K - (Cl- HCO3-)≈16mmol/L
Clinical significance
Mainly used to determine whether you suffer from metabolic acidosis
General AG>16mmol/L→Metabolic acidosis
Reduced AG value is clinically meaningless
Section 3. Simple acid-base balance disorder
Metabolic acidosis
Refers to the reduction of primary HCO3-induced pH
reason
HCO3-Directly Lost
Transgastrointestinal tract
Diarrhea, intestinal fistula or intestinal drainage
Transkidney
Type II renal tubular acidosis
Mainly proximal tubular secretion H (to preserve alkali) disorder
Use of carbonic anhydrase (CA) inhibitors in large quantities
H2CO3 in the lumen cannot dissociate CO2 and water, so the alkali cannot be reabsorbed
H increases while HCO3-buffer is lost
H generates more
Hypoxia → Anaerobic glycolysis → Lactic acid poisoning
Respiratory diseases, asphyxiation, etc.
Increased fat utilization → Increased ketone bodies → Ketoacidosis
Commonly found in diabetic patients, hunger, alcohol poisoning
H excretion disorder
Renal failure (urinary ↓)
Fixed acid can only be excreted through the kidneys
Type I renal tubular acid poisoning
Main distal tubular secretion of H (H-ATPase) disorder
Excessive intake of exogenous acids
Salicylic acid poisoning
Too much aspirin (active ingredient: acetyl-aspirin)
Acid-forming drugs containing chlorine
HCO3-diluted
Quickly input large amounts of liquid
Hyperkalemia
Potassium ions are transferred to the cell to equilibrium charge H is transferred to the cell
Metabolic acidosis can also lead to hyperkalemia
Note
Renal tubular acidosis
Alkaline urine
Other acidosis
Because of the compensatory effect of the kidney → acidic urine
Classification
AG height-enhancing type
Metabolic acidosis with increased plasma concentrations of any fixed acid other than chlorine (Cl- is a measurable anion)
Mainly seen in patients with lactic acidosis, ketoacidosis, acute renal failure and oligouria acidosis
AG normal type
Refers to HCO3-direct loss through the stomach or kidney, and Cl-compensated increase
AG=Na - (HCO3- Cl-)
Also known as hyperchlorocompensated acidosis
Mainly seen in acidosis caused by diarrhea and kidney problems
Compensation for the body
Indicator changes: AB↓, SB↓, BB↓, BE negative value increases, PH↓
Way
Blood buffering
HCO3- H =H2CO3
Intracellular buffering
H enters the cell, accompanied by K exit
There are also buffer pairs in intracellular proteins → buffer H
Compensational regulation of lungs
Increased ventilation
Compensational regulation of kidney
Increased H secretion, increased reabsorption of HCO3- and increased NH4 secretion
Impact on the body
Cardiovascular system
Myocardial contraction weakens to cause cardiac output↓
Related to Ca2 (H↑ and same-sex repulses)
H hinders intracellular Ca2 ↑
H affects Ca2 and troponin binding
Ventricular arrhythmia
Related to hyperkalemia
The vascular system's reactivity to catecholamines is reduced
Catecholamines: including epinephrine, norepinephrine, dopamine, etc.
Promote vasoconstriction (mainly peripheral resistance blood vessels)
Clinical disadvantages: hindering the emergency blood pressure increase treatment in patients with hypotension
Central nervous system
Symptoms: Inhibitory effects—consciousness disorder, lethargy, coma and even death, etc.
mechanism
Glutamate decarboxylase activity ↑, which increases the production of inhibitory neurotransmitter γ-aminobutyric acid (GABA) in the brain
Oxidative phosphorylation (biological enzyme activity ↓) is affected, and ATP synthesis is reduced
The basics of disease prevention and treatment
Treat the primary disease and remove the cause
Mild acidosis is not treated
Severe alkaline needs
NaHCO3
Replenish in batches
The amount should be small rather than large
Respiratory acidosis
Refers to the increase of primary PaCO2↑, resulting in PH↓
reason
Mainly caused by external respiratory dysfunction
Respiratory central depression
Intracerebral lesions
Drugs - anesthetics, sedatives overdose, etc.
Respiratory muscle paralysis
The main causes of death of hypokalemia
Spinal cord lesions, etc., cause damage to the phrenic nerve
Organophosphorus poisoning
Respiratory tract obstruction
Acute - Foreign objects block the organ - CO2 cannot be discharged, O2 cannot be in
Chronic-tumor, chronic respiratory diseases
Thoracic lesions
e.g. Thoracic deformation such as scoliosis affects breathing
Lung Diseases
Classification
Acute respiratory acidosis
Acute tracheal obstruction
Foreign objects in the airway
Acute cardiogenic pulmonary edema
Acute left heart failure → blood circulation in the lungs is blocked → pressure of lung circulation increases → blood in the lungs enters the alveolar veins
Respiratory arrest
Acidosis usually occurs with hypoxia
Chronic respiratory acidosis
COPD
Compensational regulation of the body
Acute respiratory acidosis
Rely on intracellular buffering
Common intracellular proteins
Hemoglobin in red blood cells
Limited buffering capacity → Acute respiratory acidosis is usually decompensated
Blood buffering is basically useless (carbonic acid buffering is useless for acidosis caused by CO2)
Renal regulation slows onset (3-4 days required)
Lung lesions are the cause
Chronic respiratory acidosis
Mainly, the kidney's hydrogen discharge increases
Impact on the body
The effect of CO2 on blood vessels
Dilate cerebrovascular causes headache
For CNS
CO2 anesthesia - headache, anxiety, irritability, insanity, lethargy, coma, etc.
The basics of disease prevention and treatment
Foreological treatment
Removal of respiratory obstruction and the use of respiratory central stimulants
Epidemiological treatment
Gradually improve ventilation function (automatic ventilation of the ventilator), but avoid excessive ventilation (prevention and treatment of respiratory alkalosis)
Avoid abuse of NaHCO3 → Prevent and treat metabolic alkalosis
Metabolic alkalosis
Refers to the increase in primary HCO3-induced pH value
reason
H Lost
Menstrual stomach loss
Gastric juice contains a lot of H
Gastric mucosal cells pass CO2 H2O→
H
Gastric fluid
HCO3-Entering Blood
"Apricot tide after meals"
Frequent vomiting (gastric juice contains a lot of H)
Transrenal loss
Diuretics
The distal urine flow speed is faster, the mechanism is the same as the loss K
Aldosterone increases
Stimulate H-ATPase in renal tubular epithelial cells
Hypokalemia
Causality and metabolic alkalosis
HCO3-excess load
Common in iatrogenic treatment of acidosis
Classification
Saline-reactive alkalosis
Replenishing saline can cure
Caused in alkalosis caused by vomiting and diuretic use (with Cl-loss)
Saline-resistant alkalosis
It is found in increased aldosterone and hypokalemia
Compensational regulation of the body
Way
Buffering of body fluids (H2CO3) and intracellular and extracellular ion exchange (intracellular H transfer to extracellular)
Compensation for lungs
Main means: inhibit the respiratory center to reduce ventilation, thereby controlling CO2 discharge
Kidney compensation
Reduce hydrogen ion secretion
Indicator changes
AB↑, SB↑, BB↑, BE positive value↑, PH↑
Impact on the body
Excited CNS
Cause: Gamma-aminobutyric acid decreases
Symptoms: restlessness, insanity, etc.
Hemoglobin oxygen separation curve left shift
That is, the affinity of Hb and O2 is enhanced
When the oxygen partial pressure is normal, Hb is not easy to release O2→deoxygenation
Free calcium in plasma↓
Muscle twitching, hand and foot twitching, convulsions, etc.
Hypokalemia
The basics of disease prevention and treatment
Brine reactivity
Supply or half a piece of salt water
Replenishment of KCl can be considered when accompanied by hypokalemia
Salt water resistance
Aldosterone supplementation drugs or potassium supplementation
Respiratory alkalosis
Concept: refers to the increase in pH due to the decrease in primary PaCO2
reason
Excessive ventilation
Hypoxemia
Lung Diseases
Probably related to hypoxemia
The role of lung stretch receptors
Direct stimulation of the respiratory center
Mental factors, brain damage
Improper use of ventilators
Classification
Acute respiratory alkalosis
Hyperthermia, hypoxemia, improper use of ventilators
Chronic respiratory alkalosis
Chronic craniocerebral diseases, chronic liver and lung diseases, etc.
Compensation adjustment
acute
H (laucic acid produced by tissue hypoxia, etc.) is moved to extracellular to neutralize extracellular HCO3-
Weak compensation ability
Chronic
Reduced compensatory hydrogen secretion in renal
Impact on the body
The effects are basically the same as metabolic alkalosis
However, the symptoms of free calcium in plasma are more significant
Dizziness, abnormal sensation around the limbs and mouth, disorders of consciousness, convulsions, etc.
The impact on CNS is also more obvious
The basics of disease prevention and treatment
Treatment of primary disease - remove the causes of hyperventilation
Acute alkaline poisoning can be considered for inhalation of mixed gas containing 5% CO2
Section 4. Mixed acid-base balance disorder
Dual acid-base balance disorder
Holic acid
Suffocation/COPD
External oxygen cannot enter the body → hypoxia → anaerobic fermentation → acid substitute
CO2 cannot be excreted in the body → acid substituted
Severe, need to be treated as soon as possible
Compensation for acid substitution involves speeding up ventilation in the lungs
Holline alkali
Long-term heavy use of diuretics and excessive ventilation
Holic acid alkali
Asphyxiation/COPD vomiting/use of diuretics
Acid substitute
Acid substitute alkali substitute
Most indicators are normal
Use AG value to judge
The pH may be normal
Note: It is impossible to have a sensational acid and a sensational acid
Triple acid-base balance disorder
Acid substitute alkali substitute
Acid substitute alkaline substitute
Difficult to determine, complex treatment
Section 2. Commonly used acid and alkali indicators
PH value
Normal 7.35-7.45
＞7.45→Alkalacterial poisoning
＜7.35→Acidtoxicity
Can't tell whether it's respiratory or metabolic
PaCO2 (partial pressure of arterial blood CO2)
Normal 33-46mmHg
＞46mmHg
Respiratory acidosis
Metabolic alkalosis after compensation
＜33mmHg
Respiratory alkalosis
Metabolic acidosis after compensation
Bicarbonate
Standard bicarbonate SB
HCO3-concentration measured in whole blood under standard conditions
Normal: 22-27mmol/L
Metabolic acidosis SB < 22mmol/L
Metabolic alkalosis SB>27mmol/L
Actual bicarbonate AB
The HCO3-concentration measured by blood samples isolated from air under actual conditions
AB=SB in normal people (the average CO2 partial pressure in normal people is 40mmHg)
Same problem as PH indicator reaction - it is impossible to tell whether it is respiratory or metabolic
AB＞SB
CO2 partial pressure in the body↑→Respiratory acidosis, metabolic alkalosis after compensation
AB＜SB
CO2 partial pressure in the body↓→Respiratory alkalosis, metabolic acidosis after compensation
Buffer alkali BB
The sum of all negative ions in the blood that have buffering capacity
Normal value: 45-51mmol/L
BB Changes
Metabolic acidosis →BB↓
Metabolic alkalosis →BB↑
Alkali remaining BE
Refers to the acid or alkali concentration required for titration of whole blood specimens with acid or alkali under standard conditions (same as SB) when pH=7.40
Normal value: -3— 3mmol/L
Acid titration → alkali residue → BE
Need for alkali titration → alkali deletion →-BE
BE changes
Metabolic acidosis
Negative value increases
Metabolic alkalosis
Positive value increases
Anion gap AG
Refers to the difference between the undetermined anion UA and the undetermined cation UC in plasma
UA
Some relatively unfixed anions
UC
Certain cations with relatively unfixed normal content
AG=UA-UC
calculate
UA Determinable Anion = UC Determinable Cation
→UA-UC=determinable cation-determinable anion
→AG=Na K - (Cl- HCO3-)≈16mmol/L
Clinical significance
Mainly used to determine whether you suffer from metabolic acidosis
General AG>16mmol/L→Metabolic acidosis
Reduced AG value is clinically meaningless
Section 3. Simple acid-base balance disorder
Metabolic acidosis
Refers to the reduction of primary HCO3-induced pH
reason
HCO3-Directly Lost
Transgastrointestinal tract
Diarrhea, intestinal fistula or intestinal drainage
Transkidney
Type II renal tubular acidosis
Mainly proximal tubular secretion H (to preserve alkali) disorder
Use of carbonic anhydrase (CA) inhibitors in large quantities
H2CO3 in the lumen cannot dissociate CO2 and water, so the alkali cannot be reabsorbed
H increases while HCO3-buffer is lost
H generates more
Hypoxia → Anaerobic glycolysis → Lactic acid poisoning
Respiratory diseases, asphyxiation, etc.
Increased fat utilization → Increased ketone bodies → Ketoacidosis
Commonly found in diabetic patients, hunger, alcohol poisoning
H excretion disorder
Renal failure (urinary ↓)
Fixed acid can only be excreted through the kidneys
Type I renal tubular acid poisoning
Main distal tubular secretion of H (H-ATPase) disorder
Excessive intake of exogenous acids
Salicylic acid poisoning
Too much aspirin (active ingredient: acetyl-aspirin)
Acid-forming drugs containing chlorine
HCO3-diluted
Quickly input large amounts of liquid
Hyperkalemia
Potassium ions are transferred to the cell to equilibrium charge H is transferred to the cell
Metabolic acidosis can also lead to hyperkalemia
Note
Renal tubular acidosis
Alkaline urine
Other acidosis
Because of the compensatory effect of the kidney → acidic urine
Classification
AG height-enhancing type
Metabolic acidosis with increased plasma concentrations of any fixed acid other than chlorine (Cl- is a measurable anion)
Mainly seen in patients with lactic acidosis, ketoacidosis, acute renal failure and oligouria acidosis
AG normal type
Refers to HCO3-direct loss through the stomach or kidney, and Cl-compensated increase
AG=Na - (HCO3- Cl-)
Also known as hyperchlorocompensated acidosis
Mainly seen in acidosis caused by diarrhea and kidney problems
Compensation for the body
Indicator changes: AB↓, SB↓, BB↓, BE negative value increases, PH↓
Way
Blood buffering
HCO3- H =H2CO3
Intracellular buffering
H enters the cell, accompanied by K exit
There are also buffer pairs in intracellular proteins → buffer H
Compensational regulation of lungs
Increased ventilation
Compensational regulation of kidney
Increased H secretion, increased reabsorption of HCO3- and increased NH4 secretion
Impact on the body
Cardiovascular system
Myocardial contraction weakens to cause cardiac output↓
Related to Ca2 (H↑ and same-sex repulses)
H hinders intracellular Ca2 ↑
H affects Ca2 and troponin binding
Ventricular arrhythmia
Related to hyperkalemia
The vascular system's reactivity to catecholamines is reduced
Catecholamines: including epinephrine, norepinephrine, dopamine, etc.
Promote vasoconstriction (mainly peripheral resistance blood vessels)
Clinical disadvantages: hindering the emergency blood pressure increase treatment in patients with hypotension
Central nervous system
Symptoms: Inhibitory effects—consciousness disorder, lethargy, coma and even death, etc.
mechanism
Glutamate decarboxylase activity ↑, which increases the production of inhibitory neurotransmitter γ-aminobutyric acid (GABA) in the brain
Oxidative phosphorylation (biological enzyme activity ↓) is affected, and ATP synthesis is reduced
The basics of disease prevention and treatment
Treat the primary disease and remove the cause
Mild acidosis is not treated
Severe alkaline needs
NaHCO3
Replenish in batches
The amount should be small rather than large
Respiratory acidosis
Refers to the increase of primary PaCO2↑, resulting in PH↓
reason
Mainly caused by external respiratory dysfunction
Respiratory central depression
Intracerebral lesions
Drugs - anesthetics, sedatives overdose, etc.
Respiratory muscle paralysis
The main causes of death of hypokalemia
Spinal cord lesions, etc., cause damage to the phrenic nerve
Organophosphorus poisoning
Respiratory tract obstruction
Acute - Foreign objects block the organ - CO2 cannot be discharged, O2 cannot be in
Chronic-tumor, chronic respiratory diseases
Thoracic lesions
e.g. Thoracic deformation such as scoliosis affects breathing
Lung Diseases
Classification
Acute respiratory acidosis
Acute tracheal obstruction
Foreign objects in the airway
Acute cardiogenic pulmonary edema
Acute left heart failure → blood circulation in the lungs is blocked → pressure of lung circulation increases → blood in the lungs enters the alveolar veins
Respiratory arrest
Acidosis usually occurs with hypoxia
Chronic respiratory acidosis
COPD
Compensational regulation of the body
Acute respiratory acidosis
Rely on intracellular buffering
Common intracellular proteins
Hemoglobin in red blood cells
Limited buffering capacity → Acute respiratory acidosis is usually decompensated
Blood buffering is basically useless (carbonic acid buffering is useless for acidosis caused by CO2)
Renal regulation slows onset (3-4 days required)
Lung lesions are the cause
Chronic respiratory acidosis
Mainly, the kidney's hydrogen discharge increases
Impact on the body
The effect of CO2 on blood vessels
Dilate cerebrovascular causes headache
For CNS
CO2 anesthesia - headache, anxiety, irritability, insanity, lethargy, coma, etc.
The basics of disease prevention and treatment
Foreological treatment
Removal of respiratory obstruction and the use of respiratory central stimulants
Epidemiological treatment
Gradually improve ventilation function (automatic ventilation of the ventilator), but avoid excessive ventilation (prevention and treatment of respiratory alkalosis)
Avoid abuse of NaHCO3 → Prevent and treat metabolic alkalosis
Metabolic alkalosis
Refers to the increase in primary HCO3-induced pH value
reason
H Lost
Menstrual stomach loss
Gastric juice contains a lot of H
Gastric mucosal cells pass CO2 H2O→
H
Gastric fluid
HCO3-Entering Blood
"Apricot tide after meals"
Frequent vomiting (gastric juice contains a lot of H)
Transrenal loss
Diuretics
The distal urine flow speed is faster, the mechanism is the same as the loss K
Aldosterone increases
Stimulate H-ATPase in renal tubular epithelial cells
Hypokalemia
Causality and metabolic alkalosis
HCO3-excess load
Common in iatrogenic treatment of acidosis
Classification
Saline-reactive alkalosis
Replenishing saline can cure
Caused in alkalosis caused by vomiting and diuretic use (with Cl-loss)
Saline-resistant alkalosis
It is found in increased aldosterone and hypokalemia
Compensational regulation of the body
Way
Buffering of body fluids (H2CO3) and intracellular and extracellular ion exchange (intracellular H transfer to extracellular)
Compensation for lungs
Main means: inhibit the respiratory center to reduce ventilation, thereby controlling CO2 discharge
Kidney compensation
Reduce hydrogen ion secretion
Indicator changes
AB↑, SB↑, BB↑, BE positive value↑, PH↑
Impact on the body
Excited CNS
Cause: Gamma-aminobutyric acid decreases
Symptoms: restlessness, insanity, etc.
Hemoglobin oxygen separation curve left shift
That is, the affinity of Hb and O2 is enhanced
When the oxygen partial pressure is normal, Hb is not easy to release O2→deoxygenation
Free calcium in plasma↓
Muscle twitching, hand and foot twitching, convulsions, etc.
Hypokalemia
The basics of disease prevention and treatment
Brine reactivity
Supply or half a piece of salt water
Replenishment of KCl can be considered when accompanied by hypokalemia
Salt water resistance
Aldosterone supplementation drugs or potassium supplementation
Respiratory alkalosis
Concept: refers to the increase in pH due to the decrease in primary PaCO2
reason
Excessive ventilation
Hypoxemia
Lung Diseases
Probably related to hypoxemia
The role of lung stretch receptors
Direct stimulation of the respiratory center
Mental factors, brain damage
Improper use of ventilators
Classification
Acute respiratory alkalosis
Hyperthermia, hypoxemia, improper use of ventilators
Chronic respiratory alkalosis
Chronic craniocerebral diseases, chronic liver and lung diseases, etc.
Compensation adjustment
acute
H (laucic acid produced by tissue hypoxia, etc.) is moved to extracellular to neutralize extracellular HCO3-
Weak compensation ability
Chronic
Reduced compensatory hydrogen secretion in renal
Impact on the body
The effects are basically the same as metabolic alkalosis
However, the symptoms of free calcium in plasma are more significant
Dizziness, abnormal sensation around the limbs and mouth, disorders of consciousness, convulsions, etc.
The impact on CNS is also more obvious
The basics of disease prevention and treatment
Treatment of primary disease - remove the causes of hyperventilation
Acute alkaline poisoning can be considered for inhalation of mixed gas containing 5% CO2
Section 4. Mixed acid-base balance disorder
Dual acid-base balance disorder
Holic acid
Suffocation/COPD
External oxygen cannot enter the body → hypoxia → anaerobic fermentation → acid substitute
CO2 cannot be excreted in the body → acid substituted
Severe, need to be treated as soon as possible
Compensation for acid substitution involves speeding up ventilation in the lungs
Holline alkali
Long-term heavy use of diuretics and excessive ventilation
Holic acid alkali
Asphyxiation/COPD vomiting/use of diuretics
Acid substitute
Acid substitute alkali substitute
Most indicators are normal
Use AG value to judge
The pH may be normal
Note: It is impossible to have a sensational acid and a sensational acid
Triple acid-base balance disorder
Acid substitute alkali substitute
Acid substitute alkaline substitute
Difficult to determine, complex treatment