MindMap Gallery Pathophysiology - Water and electrolyte disorders
Water and electrolyte disorders are an important manifestation of the imbalance in the human body's internal environment, involving abnormal metabolism of key ions such as potassium and sodium. Hyperkalemia and hypokalemia are caused by serum potassium ion concentrations above 55mmol/L or below 35mmol/L, respectively, which affect the functions of important organs such as the heart and skeletal muscle. Abnormal serum sodium concentrations are divided into hypernatremia and hyponatremia, which are related to osmotic pressure imbalance or fluid volume disorder, respectively. Aldosterone and ADH hormones play a key role in the regulation of sodium and water balance. Treatment needs to target the cause, such as dialysis, insulin injection, etc., to restore the internal environmental homeostasis. Understanding the physiological basis and impact of these disorders can help to identify and intervene effectively in the early stage.
Edited at 2025-03-10 15:34:50Rumi: 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.
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.
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.
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.
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.
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.
Section 1. Physiological Basics
body fluid
content
Adult men make up 60% of their weight
40% intracellular
20% extracellular
15% intertituent fluid
5% plasma
Adult women make up 50% of their body weight (less fat)
80% of infants and toddlers
composition
water
The daily inlet and outflow volume is about 2000-2500ml
Source of water
Drinking water 1000-1500ml
Food contains water 700-1200ml
Endogenous water 300ml
Water produced by biochemical reactions in the body
Water excretion
Urine
Average daily 1200-1500ml
Urine volume reflects renal function
Feces: about 150ml/day
Exhale about 350ml/day
Skin: about 500ml/day
Sweat, evaporate
Solute
Non-electrolytes
Electrolyte
main
Positive ions
Na, K, Ca2
Negative ions
Cl-, HCO3-
Main functions
Maintain osmotic pressure and acid-base balance of body fluids
Maintain resting potentials and participating in action potentials of nerves, muscles, and cardiomyocytes
Participate in physiological activities such as metabolism
Water balance adjustment
Thirst
Increased plasma osmotic pressure causes thirst
ADH antidiuretic hormone
Plasma osmotic pressure
Increase secretion
Reduce secretion
Effective circulating blood volume
Reduce secretion increase
Increased secretion
Sodium balance regulation
Aldosterone
Mainly produced by the adrenal cortex
Promote the reabsorption of sodium by the original flexure tubules
Extract potassium and sodium (it will retain water while maintaining sodium)
Increases in effective circulating blood volume
Mechanism: Renin-angiotensin-aldosterone system
Water and electrolyte disorders
Section 1. Physiological Basics
body fluid
content
Adult men make up 60% of their weight
40% intracellular
20% extracellular
15% intertituent fluid
5% plasma
Adult women make up 50% of their body weight (less fat)
80% of infants and toddlers
composition
water
The daily inlet and outflow volume is about 2000-2500ml
Source of water
Drinking water 1000-1500ml
Food contains water 700-1200ml
Endogenous water 300ml
Water produced by biochemical reactions in the body
Water excretion
Urine
Average daily 1200-1500ml
Urine volume reflects renal function
Feces: about 150ml/day
Exhale about 350ml/day
Skin: about 500ml/day
Sweat, evaporate
Solute
Non-electrolytes
Electrolyte
main
Positive ions
Na, K, Ca2
Negative ions
Cl-, HCO3-
Main functions
Maintain osmotic pressure and acid-base balance of body fluids
Maintain resting potentials and participating in action potentials of nerves, muscles, and cardiomyocytes
Participate in physiological activities such as metabolism
Water balance adjustment
Thirst
Increased plasma osmotic pressure causes thirst
ADH antidiuretic hormone
Plasma osmotic pressure
Increase secretion
Reduce secretion
Effective circulating blood volume
Reduce secretion increase
Increased secretion
Sodium balance regulation
Aldosterone
Mainly produced by the adrenal cortex
Promote the reabsorption of sodium by the original flexure tubules
Extract potassium and sodium (it will retain water while maintaining sodium)
Increases in effective circulating blood volume
Mechanism: Renin-angiotensin-aldosterone system
Section 2. Disorders in water and sodium metabolism
Normal blood sodium concentration-disordered fluid volume balance
Low volume dysemia
Insufficient extracellular fluid capacity
Causes
Extra-renal loss
Vomiting, diarrhea, burns, etc.
Transrenal loss
Acute renal failure polyuria
Oligouric acute renal failure is common - early oligouria (<400ml/d)
The urine volume increased after treatment, but the renal tubular reabsorption function did not fully recover → a large amount of water and sodium were lost
Certain chronic kidney disease
Adrenal cortex insufficiency
→Insufficient Aldosterone secretion
Long-term use of diuretics
Influence
Mild loss can be compensated for repair
Reduced cardiac output → lowered blood pressure → sympathetic nerve excitation → recovery of cardiac output
Severe low volumeemia can cause shock
The basics of treatment
First - isotonic salt water 0.9% NaCl
After - Appropriate half a piece of salt water 0..45% NaCl
Promotes cells to absorb water, brings out toxic substances in the cell, and promotes cell recovery
Excessive extracellular fluid capacity
High volume dysemia
Edema
Causes
Congestive heart failure
Increased venous pressure
Cirrhosis
Protein synthesis decreases, plasma colloid osmotic pressure↓
Nephrotic syndrome
Proteinuria → plasma colloid osmotic pressure↓
Malnutrition
......
Generation mechanism
Imbalance of fluid exchange in and out of the body - sodium water retention
Glomerular filtration rate decreases
Extensive glomerulial lesions
Effective circulating blood volume reduction
Reabsorption enhancement of proximal curvature tubules
ANP atrial natriuretic peptide/natriuretic hormone reduction
Reabsorption enhancement of distal curved tubules
Aldosterone increase
ADH increases
Abnormal distribution of internal and external blood vessels-Tissue fluid generation>Reflux
Cap. In addition of hydrostatic pressure
Congestive heart failure → Intravenous system blood stasis
Reduced plasma colloid osmotic pressure
Mainly related to protein concentration
Cirrhosis
Protein urine
Malnutrition, etc.
Cap. Enhanced permeability
Protein, etc. enters the tissue fluid
Lymph system return impeded
The basics of treatment
Limit sodium intake
Choose appropriate diuretics
Abnormal serum sodium concentration-osmotic pressure imbalance
Hyponatremia
The concentration of blood sodium is less than 130mmol/L
Causes
Water retention
Also known as "dilution hyponatremia" or "water poisoning"
Drinking too much water
Mental illness, etc.
Excessive secretion of ADH
Central injury
Lung tumors may also produce ADH
Sodium loss (> water loss)
Also known as "consumed hyponatremia", hypotonic dehydration
Renal loss
Mainly seen in people who use diuretics for a long time and have a low salt diet
Extra-renal loss
Vomiting, diarrhea, and a lot of sweating
Influence
Mild
Decreased taste, muscle spasms, headaches, nausea, etc.
Severe (<120mmol/L)
Coma, reflex disappear, etc.
The basics of treatment
Dilute hyponatremia
Limit water
Consumptive hyponatremia
Sodium supplement
Generally, normal saline is supplemented, and hypertonic saline can be used in severe cases.
Hypernatremia
The concentration of serum sodium is higher than 150mmol/L; osmotic pressure >310mmol/L
Causes
Hypersensitivity dehydration
Loss of water > Loss of sodium
way
Extra-renal loss
Fever, excessive ventilation, heavy sweating, severe vomiting and diarrhea, etc.
Transrenal loss
ADH
Generate reduction
Central diabetic collapse
Weak effect
Peripheral dialysis
Permeable dialysis
Osmotic pressure in the renal tubular lumen↑
diabetes
Intravenous mannol injection during cerebral edema
Too much sodium intake
Eat salt by accident, etc.
Influence
Thirsty, flushed skin. Dry mouth and tongue, etc.
Brain cell dehydration occurs in severe cases
Tired brain, lethargy, coma and even death
The basics of treatment
Simple water loss
Hydrating, intravenous hypotonic glucose
Reduced blood volume
First replenish the blood volume of isotonic saline, and then correct the hypotonic solution.
Increased blood volume
Natriuretic agent, intravenous supplementation of hypotonic glucose
Section 3 Potassium ion disorder
Hypokalemia
concept
Serum potassium ion concentration <3.5mmol/L
Differentiate from "potassium deficiency" - lack of potassium ions in cells
Hypokalemia ≠ potassium deficiency
Causes
Reduced food intake
Excessive discharge
Transgastrointestinal loss
Vomiting diarrhea, etc.
Transrenal loss
Long-term use of diuretics (to increase distal urine flow rate)
Osmotic diuretic - diabetes, etc., make the osmotic pressure of the prourinary urine↑
Increased mineralocorticoids (aldosterone)
Renal tubular acidosis
H cannot be discharged →Secondary K is discharged ↑
Transdermal loss
Sweat a lot
K distribution is abnormal, K is transferred into cells
Acute alkalosis
Alkalosis → Extracellular H ↓→ Intracellular H turns to extracellular → It is ionic equilibrium, K enters the cell
High doses of insulin and glucose
Insulin → Promote glucose to synthesize glycogen → K is required to participate
Hypokalemia-type periodic paralysis
Genetic diseases, periodic diseases
Hyperthyroidism, barium poisoning, etc.
Influence
Central nervous system
Symptoms: listless, indifference, coma
Brain cells: excitability, ATP energy supply insufficient
Cardiovascular system
Abnormal heart rate
The electrophysiological characteristics of cardiomyocytes are disturbed
Skeletal muscle
Weakness or even paralysis
Respiratory muscle paralysis—the main cause of death
Gastrointestinal tract
Gastrointestinal movement weakens
kidney
Impaired concentration function, polyuria, low specific gravity urine
The basics of treatment
Mild: Eat foods rich in potassium
serious
Potassium supplements only when the urine volume is normal to prevent fatal hyperkalemia
Best oral
Rather than be insignificant than be indiscriminate, step by step
Intravenous drops
Low concentration 30-40mmol/L
Slow drop speed 10-20mmol/L
Need to be under ECG monitoring (prevent hyperkalemia)
Hyperkalemia
Serum potassium ion concentration >5.5mmol/L
Causes
Too much intake
Excessive potassium intake due to renal insufficiency
Idiopathic
Input a large amount of blood in stock, etc.
Reduced discharge
Acute renal failure oliguria
Adrenal cortex insufficiency
Aldosterone reduction
Use potassium-saving diuretics in large quantities
Intracellular K escape
Large amount of hemolysis, tissue necrosis
e.g.Squeeze injury syndrome
Acidosis
Insulin deficiency
Hyperkalemia-type periodic paralysis
Family genetic disease
Influence
heart
Mild hyperkalemia-cardiomyocyte excitability↑; severe hyperkalemia-cardiomyocyte↓
symptom
Severe atrioventricular block
Ventria fibrillation
Cardiac arrest
The main cause of death
Skeletal muscle
Mild
Muscle tremor, abnormal sensation
high
Weakness, paralysis
The basics of treatment
Against potassium ion toxicity
Temporary, emergency
(Same-sexual repulsion) → Enter Na, Ca2, etc.
Injection of high doses of insulin and glucose
Temporary, emergency
Make a large amount of K into the cell
Dialysis
Hemodialysis
Peritoneal dialysis
Section 2. Disorders in water and sodium metabolism
Normal blood sodium concentration-disordered fluid volume balance
Low volume dysemia
Insufficient extracellular fluid capacity
Causes
Extra-renal loss
Vomiting, diarrhea, burns, etc.
Transrenal loss
Acute renal failure polyuria
Oligouric acute renal failure is common - early oligouria (<400ml/d)
The urine volume increased after treatment, but the renal tubular reabsorption function did not fully recover → a large amount of water and sodium were lost
Certain chronic kidney disease
Adrenal cortex insufficiency
→Insufficient Aldosterone secretion
Long-term use of diuretics
Influence
Mild loss can be compensated for repair
Reduced cardiac output → lowered blood pressure → sympathetic nerve excitation → recovery of cardiac output
Severe low volumeemia can cause shock
The basics of treatment
First - isotonic salt water 0.9% NaCl
After - Appropriate half a piece of salt water 0..45% NaCl
Promotes cells to absorb water, brings out toxic substances in the cell, and promotes cell recovery
Excessive extracellular fluid capacity
High volume dysemia
Edema
Causes
Congestive heart failure
Increased venous pressure
Cirrhosis
Protein synthesis decreases, plasma colloid osmotic pressure↓
Nephrotic syndrome
Proteinuria → plasma colloid osmotic pressure↓
Malnutrition
......
Generation mechanism
Imbalance of fluid exchange in and out of the body - sodium water retention
Glomerular filtration rate decreases
Extensive glomerulial lesions
Effective circulating blood volume reduction
Reabsorption enhancement of proximal curvature tubules
ANP atrial natriuretic peptide/natriuretic hormone reduction
Reabsorption enhancement of distal curved tubules
Aldosterone increase
ADH increases
Abnormal distribution of internal and external blood vessels-Tissue fluid generation>Reflux
Cap. In addition of hydrostatic pressure
Congestive heart failure → Intravenous system blood stasis
Reduced plasma colloid osmotic pressure
Mainly related to protein concentration
Cirrhosis
Protein urine
Malnutrition, etc.
Cap. Enhanced permeability
Protein, etc. enters the tissue fluid
Lymph system return impeded
The basics of treatment
Limit sodium intake
Choose appropriate diuretics
Abnormal serum sodium concentration-osmotic pressure imbalance
Hyponatremia
The concentration of blood sodium is less than 130mmol/L
Causes
Water retention
Also known as "dilution hyponatremia" or "water poisoning"
Drinking too much water
Mental illness, etc.
Excessive secretion of ADH
Central injury
Lung tumors may also produce ADH
Sodium loss (> water loss)
Also known as "consumed hyponatremia", hypotonic dehydration
Renal loss
Mainly seen in people who use diuretics for a long time and have a low salt diet
Extra-renal loss
Vomiting, diarrhea, and a lot of sweating
Influence
Mild
Decreased taste, muscle spasms, headaches, nausea, etc.
Severe (<120mmol/L)
Coma, reflex disappear, etc.
The basics of treatment
Dilute hyponatremia
Limit water
Consumptive hyponatremia
Sodium supplement
Generally, normal saline is supplemented, and hypertonic saline can be used in severe cases.
Hypernatremia
The concentration of serum sodium is higher than 150mmol/L; osmotic pressure >310mmol/L
Causes
Hypersensitivity dehydration
Loss of water > Loss of sodium
way
Extra-renal loss
Fever, excessive ventilation, heavy sweating, severe vomiting and diarrhea, etc.
Transrenal loss
ADH
Generate reduction
Central diabetic collapse
Weak effect
Peripheral dialysis
Permeable dialysis
Osmotic pressure in the renal tubular lumen↑
diabetes
Intravenous mannol injection during cerebral edema
Too much sodium intake
Eat salt by accident, etc.
Influence
Thirsty, flushed skin. Dry mouth and tongue, etc.
Brain cell dehydration occurs in severe cases
Tired brain, lethargy, coma and even death
The basics of treatment
Simple water loss
Hydrating, intravenous hypotonic glucose
Reduced blood volume
First replenish the blood volume of isotonic saline, and then correct the hypotonic solution.
Increased blood volume
Natriuretic agent, intravenous supplementation of hypotonic glucose
Section 3 Potassium ion disorder
Hypokalemia
concept
Serum potassium ion concentration <3.5mmol/L
Differentiate from "potassium deficiency" - lack of potassium ions in cells
Hypokalemia ≠ potassium deficiency
Causes
Reduced food intake
Excessive discharge
Transgastrointestinal loss
Vomiting diarrhea, etc.
Transrenal loss
Long-term use of diuretics (to increase distal urine flow rate)
Osmotic diuretic - diabetes, etc., make the osmotic pressure of the prourinary urine↑
Increased mineralocorticoids (aldosterone)
Renal tubular acidosis
H cannot be discharged →Secondary K is discharged ↑
Transdermal loss
Sweat a lot
K distribution is abnormal, K is transferred into cells
Acute alkalosis
Alkalosis → Extracellular H ↓→ Intracellular H turns to extracellular → It is ionic equilibrium, K enters the cell
High doses of insulin and glucose
Insulin → Promote glucose to synthesize glycogen → K is required to participate
Hypokalemia-type periodic paralysis
Genetic diseases, periodic diseases
Hyperthyroidism, barium poisoning, etc.
Influence
Central nervous system
Symptoms: listless, indifference, coma
Brain cells: excitability, ATP energy supply insufficient
Cardiovascular system
Abnormal heart rate
The electrophysiological characteristics of cardiomyocytes are disturbed
Skeletal muscle
Weakness or even paralysis
Respiratory muscle paralysis—the main cause of death
Gastrointestinal tract
Gastrointestinal movement weakens
kidney
Impaired concentration function, polyuria, low specific gravity urine
The basics of treatment
Mild: Eat foods rich in potassium
serious
Potassium supplements only when the urine volume is normal to prevent fatal hyperkalemia
Best oral
Rather than be insignificant than be indiscriminate, step by step
Intravenous drops
Low concentration 30-40mmol/L
Slow drop speed 10-20mmol/L
Need to be under ECG monitoring (prevent hyperkalemia)
Hyperkalemia
Serum potassium ion concentration >5.5mmol/L
Causes
Too much intake
Excessive potassium intake due to renal insufficiency
Idiopathic
Input a large amount of blood in stock, etc.
Reduced discharge
Acute renal failure oliguria
Adrenal cortex insufficiency
Aldosterone reduction
Use potassium-saving diuretics in large quantities
Intracellular K escape
Large amount of hemolysis, tissue necrosis
e.g.Squeeze injury syndrome
Acidosis
Insulin deficiency
Hyperkalemia-type periodic paralysis
Family genetic disease
Influence
heart
Mild hyperkalemia-cardiomyocyte excitability↑; severe hyperkalemia-cardiomyocyte↓
symptom
Severe atrioventricular block
Ventria fibrillation
Cardiac arrest
The main cause of death
Skeletal muscle
Mild
Muscle tremor, abnormal sensation
high
Weakness, paralysis
The basics of treatment
Against potassium ion toxicity
Temporary, emergency
(Same-sexual repulsion) → Enter Na, Ca2, etc.
Injection of high doses of insulin and glucose
Temporary, emergency
Make a large amount of K into the cell
Dialysis
Hemodialysis
Peritoneal dialysis