CA

Fluid and Electrolyte Balance Summary

Fluid and Electrolyte Balance

Introduction

  • Fluid and electrolyte homeostasis

  • Water balance

  • Sodium balance and extracellular fluid connection

  • Potassium balance

  • Behavioral mechanisms controlling salt and water

  • Integration control of volume and osmolarity

  • Acid-base balance examples

Water Balance

  • Homeostasis depends on:

    • Kidneys

    • Respiratory system

    • Cardiovascular system

  • Thirst and water craving are behavioral mechanisms linked to physiological needs via the hypothalamus.

  • The hypothalamus connects behavioral and physical aspects (e.g., stress and sickness, hunger and sugar needs).

  • Kidneys conserve water but cannot create it.

Blood Pressure and Volume Relationship

  • Decreased blood pressure and volume response:

    • Volume receptors in atria and carotid/aortic baroreceptors.

    • Sympathetic innervation increases heart rate and cardiac output.

    • Vasoconstriction increases blood pressure.

Hypothalamus and Osmolarity

  • Hypothalamus contains osmoreceptors.

  • Low volume leads to high osmolarity, triggering ADH (Antidiuretic Hormone) formation.

  • ADH causes kidneys to conserve water.

  • Hypothalamus triggers thirst, increasing fluid intake and blood pressure.

  • Increased blood volume increases blood pressure.

    • Detected by beta receptors triggering parasympathetic response.

    • Reduced cardiac output and vasodilation lower blood pressure.

  • No ADH production leads to water excretion in urine, reducing volume and blood pressure.

  • Water balance is maintained by the urinary system, requiring external water intake.

Glomerular Filtration Rate (GFR)

  • High volume increases blood pressure and GFR, leading to more fluid in urine.

  • Low volume decreases GFR, conserving water until normal levels are reached.

Urine Concentration in Nephrons

  • Medulla of kidneys sets threshold for what exits the tubular system.

  • Higher osmolarity in the medulla concentrates urine.

  • Fluid in the descending loop of Henle loses water via osmosis.

  • Cells in the thick ascending limb are water-impermeable, transporting sodium out to reduce osmolarity.

  • Distal nephrons control water reabsorption via hormones like ADH.

  • Diuresis is excess water removal; diuretics promote urine excretion for high blood pressure or heart failure.

  • Membrane recycling allows vasopressin (ADH) to control water permeability in distal tubules and collecting ducts via aquaporins (water holes).

  • Nocturnal anuresis is bed wetting.

Nephron Function and Osmolarity

  • The medullary area has higher osmolarity.

  • Water reabsorption occurs due to osmotic/oncotic pressure.

  • Isotonicity or iso-osmolarity is maintained.

  • The ascending limb pumps ions (e.g., sodium) out without water.

  • The distal part of the tubule and collecting ducts reabsorb water under ADH control.

The Three Musketeers

1. Vasopressin (ADH)
  • Vasopressin = vasoconstriction (increases blood pressure)

  • Antidiuretic hormone = prevents urination (increases volume and pressure)

  • Triggered by conditions that drop blood pressure or reduce water (e.g., dehydration).

  • Hypothalamic osmoreceptors sense these conditions.

  • Made in hypothalamus, released by posterior pituitary gland.

  • Works on renal collecting ducts & distal tubules for water reabsorption.

Countercurrent Multiplier of Vasa Recta
  • Ascending limb pumps sodium out, water follows, diluting the medulla.

  • Renal system uses a countercurrent exchange system.

  • Vasa recta (straight blood vessels) remove water from the medulla to prevent dilution.

  • Fluid in the descending loop of Henle loses water to the medulla.

  • As fluid ascends, sodium, potassium, and chloride are pumped out, reducing osmolarity.

  • Vasa recta takes up water to maintain osmolarity.

2. Aldosterone
  • Responsible for sodium reabsorption; water follows.

  • Increases blood pressure.

  • Activates B cells of collecting ducts to reabsorb sodium, excreting potassium.

  • High aldosterone = increased sodium, decreased potassium.

  • Triggered by low blood pressure.

  • Stimulates adrenal cortex to produce aldosterone (a steroid).

3. Angiotensin II
  • Increases blood pressure.

  • Stimulates aldosterone synthesis.

  • Increases vasopressin release.

  • Increases thirst.

  • Indirect effect on the cardiovascular center (medulla oblongata).

  • Increases sympathetic innervation and cardiac output.

  • Vasoconstriction (primary function).

  • Sodium and hydrogen ion exchanger.

Renin-Angiotensin-Aldosterone System (RAAS)
  • Angiotensin II Functions:

    • Vasoconstriction.

    • Activates cardiovascular center and induces sympathetic innervation.

    • Increases vasopressin release and thirst.

    • Stimulates adrenal cortex to produce aldosterone.

    • Increases sodium and water reabsorption.

  • Production and Activation:

    • Angiotensinogen (inactive) is made in the liver.

    • Renin (from juxtaglomerular cells in kidneys) activates angiotensinogen into angiotensin I in response to decreased GFR.

    • Angiotensin Converting Enzyme (ACE) converts angiotensin I into angiotensin II in the blood vessels (especially in the lungs).

  • ACE Inhibitors: block ACE to slow down the production of angiotensin II, treating high blood pressure.

Potassium Balance

  • Potassium, kalemia, cardiac.

  • Aldosterone reabsorbs sodium but excretes potassium.

  • Hyperkalemia: Too much potassium, kidney has to kick out the sodium - causes:

    • Kidney diseases

    • Diarrhea

    • Diuretics

  • Hypokalemia: Low potassium level - leads to:

    • Muscle weakness, failure of the respiratory muscle and heart.

  • Hyperkalemia can lead into cardiac arrhythmias.

Acid-Base Balance Refresher

  • Normal plasma pH: 7.38 - 7.42

  • Controlled by hydrogen ion concentration.

  • pH modulates enzyme functionality; abnormal pH affects protein structure and nervous system.

  • Acidosis: Neurons become less excitable; CNS depression.

  • Alkalosis: Hyper-excitability.

  • pH disturbances are associated with potassium disturbances.

  • Kidneys pump potassium and hydrogen oppositely.

    • Example: Hyperkalemia leads to losing hydrogen ion, or acid, which leads to metabolic alkalosis.

Factors Shifting pH

  • Diet (fatty acids, amino acids)

  • Breathing (carbon dioxide from metabolism)

  • Water (forms carbonic acid)

  • Production of lactic acid and ketoacidosis

Control Mechanisms
  • Buffer system (bicarbonate in extracellular fluid)

  • Proteins, hemoglobin, phosphates in cells

  • Phosphate and ammonia in urine

  • Respiratory system (ventilation)

  • Renal system (excretion of hydrogen)

  • Hyperventilation: Washing off carbon dioxide, losing acid (respiratory alkalosis).

Buffers and Ventilation

  • Buffers control moderate pH changes.

  • Cellular proteins, phosphate ions, hemoglobin, and bicarbonate balance pH.

  • Ventilation rapidly corrects 75% of disturbances but cannot maintain long-term.

Renal Regulation

  • Receptor-mediated endocytosis.

  • Directly excretes or reabsorbs hydrogen ions.

  • Indirectly changes the rate at which bicarb buffer is reabsorbed or excreted.

Introduction
  • Fluid and electrolyte homeostasis are crucial for maintaining cellular function, nerve impulse transmission, and overall physiological balance.

  • Water balance involves the regulation of water intake and output to maintain optimal hydration levels.

  • Sodium balance is closely linked to extracellular fluid volume, influencing blood pressure and fluid distribution.

  • Potassium balance is essential for proper cardiac and muscle function, with imbalances potentially leading to life-threatening arrhythmias.

  • Behavioral mechanisms, such as thirst and salt cravings, play a vital role in maintaining fluid and electrolyte balance by encouraging intake when needed.

  • Integration control mechanisms, including hormones and neural pathways, coordinate fluid and electrolyte regulation to maintain homeostasis.

  • Acid-base balance is critical for enzyme function and overall metabolic processes; imbalances can have severe physiological consequences.

Water Balance
  • Homeostasis depends on:

    • Kidneys: Regulate water excretion and reabsorption.

    • Respiratory system: Influences water loss through breathing.

    • Cardiovascular system: Maintains blood pressure and fluid distribution.

  • Thirst and water craving are behavioral mechanisms linked to physiological needs via the hypothalamus.

  • The hypothalamus connects behavioral and physical aspects (e.g., stress and sickness, hunger and sugar needs), ensuring that hydration and electrolyte levels are maintained in response to various stimuli.

  • Kidneys conserve water but cannot create it, highlighting the importance of external water intake.

Blood Pressure and Volume Relationship
  • Decreased blood pressure and volume response:

    • Volume receptors in atria and carotid/aortic baroreceptors detect changes and initiate compensatory mechanisms.

    • Sympathetic innervation increases heart rate and cardiac output to raise blood pressure.

    • Vasoconstriction increases blood pressure by narrowing blood vessels.

Hypothalamus and Osmolarity
  • Hypothalamus contains osmoreceptors that monitor blood osmolarity, triggering appropriate responses to maintain fluid balance.

  • Low volume leads to high osmolarity, triggering ADH (Antidiuretic Hormone) formation, which promotes water conservation by the kidneys.

  • ADH causes kidneys to conserve water by increasing water reabsorption in the collecting ducts.

  • Hypothalamus triggers thirst, increasing fluid intake and blood pressure, thus restoring normal fluid volume.

  • Increased blood volume increases blood pressure.

    • Detected by beta receptors triggering parasympathetic response, which helps to lower blood pressure.

    • Reduced cardiac output and vasodilation lower blood pressure, maintaining balance.

  • No ADH production leads to water excretion in urine, reducing volume and blood pressure, which can occur when the body is adequately hydrated or overhydrated.

  • Water balance is maintained by the urinary system, requiring external water intake to compensate for daily losses and bodily functions.

Glomerular Filtration Rate (GFR)
  • High volume increases blood pressure and GFR, leading to more fluid in urine as the kidneys filter excess fluid.

  • Low volume decreases GFR, conserving water until normal levels are reached, ensuring that the body retains necessary fluids.

Urine Concentration in Nephrons
  • Medulla of kidneys sets threshold for what exits the tubular system, determining the final concentration of urine.

  • Higher osmolarity in the medulla concentrates urine, allowing the kidneys to excrete waste with minimal water loss.

  • Fluid in the descending loop of Henle loses water via osmosis as it moves into the hyperosmotic medulla.

  • Cells in the thick ascending limb are water-impermeable, transporting sodium out to reduce osmolarity, creating a concentration gradient.

  • Distal nephrons control water reabsorption via hormones like ADH, fine-tuning urine concentration based on the body’s needs.

  • Diuresis is excess water removal; diuretics promote urine excretion for high blood pressure or heart failure by interfering with sodium and water reabsorption.

  • Membrane recycling allows vasopressin (ADH) to control water permeability in distal tubules and collecting ducts via aquaporins (water holes), adjusting water reabsorption based on hydration status.

  • Nocturnal anuresis is bed wetting, often due to inadequate ADH production or responsiveness.

Nephron Function and Osmolarity
  • The medullary area has higher osmolarity, facilitating water reabsorption.

  • Water reabsorption occurs due to osmotic/oncotic pressure, driving water from the tubules into the surrounding tissues.

  • Isotonicity or iso-osmolarity is maintained in the loop of Henle to optimize water and solute reabsorption.

  • The ascending limb pumps ions (e.g., sodium) out without water, contributing to the high osmolarity of the medulla.

  • The distal part of the tubule and collecting ducts reabsorb water under ADH control, allowing for precise regulation of urine concentration.

The Three Musketeers
1. Vasopressin (ADH)
  • Vasopressin = vasoconstriction (increases blood pressure) by constricting blood vessels.

  • Antidiuretic hormone = prevents urination (increases volume and pressure) by promoting water reabsorption in the kidneys.

  • Triggered by conditions that drop blood pressure or reduce water (e.g., dehydration), ensuring the body conserves water when needed.

  • Hypothalamic osmoreceptors sense these conditions, initiating ADH release.

  • Made in hypothalamus, released by posterior pituitary gland, allowing for quick and coordinated response.

  • Works on renal collecting ducts & distal tubules for water reabsorption, increasing water retention.

Countercurrent Multiplier of Vasa Recta
  • Ascending limb pumps sodium out, water follows, diluting the medulla, which is essential for creating the concentration gradient.

  • Renal system uses a countercurrent exchange system in the loop of Henle to maximize water reabsorption.

  • Vasa recta (straight blood vessels) remove water from the medulla to prevent dilution, maintaining the high osmolarity needed for water reabsorption.

  • Fluid in the descending loop of Henle loses water to the medulla, concentrating the tubular fluid.

  • As fluid ascends, sodium, potassium, and chloride are pumped out, reducing osmolarity, which helps to create a dilute filtrate.

  • Vasa recta takes up water to maintain osmolarity, preventing the medulla from becoming too dilute.

2. Aldosterone
  • Responsible for sodium reabsorption; water follows, increasing blood volume and maintaining electrolyte balance.

  • Increases blood pressure by increasing sodium and water retention.

  • Activates B cells of collecting ducts to reabsorb sodium, excreting potassium, regulating electrolyte balance.

  • High aldosterone = increased sodium, decreased potassium, affecting blood pressure and cardiac function.

  • Triggered by low blood pressure, initiating a cascade of hormonal responses to increase blood volume and pressure.

  • Stimulates adrenal cortex to produce aldosterone (a steroid), ensuring long-term regulation of sodium and potassium levels.

3. Angiotensin II
  • Increases blood pressure through multiple mechanisms.

  • Stimulates aldosterone synthesis, enhancing sodium and water reabsorption.

  • Increases vasopressin release, further promoting water retention.

  • Increases thirst, encouraging fluid intake to raise blood volume.

  • Indirect effect on the cardiovascular center (medulla oblongata), influencing sympathetic and parasympathetic activity.

  • Increases sympathetic innervation and cardiac output, raising blood pressure and maintaining perfusion.

  • Vasoconstriction (primary function), narrowing blood vessels to elevate blood pressure.

  • Sodium and hydrogen ion exchanger, regulating pH and electrolyte balance.

Renin-Angiotensin-Aldosterone System (RAAS)
  • Angiotensin II Functions:

    • Vasoconstriction, increasing blood pressure.

    • Activates cardiovascular center and induces sympathetic innervation, enhancing cardiac output and blood pressure.

    • Increases vasopressin release and thirst, promoting fluid retention and intake.

    • Stimulates adrenal cortex to produce aldosterone, increasing sodium and water reabsorption.

    • Increases sodium and water reabsorption, expanding blood volume and maintaining electrolyte balance.

  • Production and Activation:

    • Angiotensinogen (inactive) is made in the liver and is the precursor to angiotensin II.

    • Renin (from juxtaglomerular cells in kidneys) activates angiotensinogen into angiotensin I in response to decreased GFR, initiating the RAAS cascade.

    • Angiotensin Converting Enzyme (ACE) converts angiotensin I into angiotensin II in the blood vessels (especially in the lungs), completing the activation process.

  • ACE Inhibitors: block ACE to slow down the production of angiotensin II, treating high blood pressure by reducing vasoconstriction and fluid retention.

Potassium Balance
  • Potassium, kalemia, cardiac: Potassium levels are critical for proper cardiac function, and imbalances can lead to arrhythmias.

  • Aldosterone reabsorbs sodium but excretes potassium, maintaining electrolyte balance.

  • Hyperkalemia: Too much potassium, kidney has to kick out the sodium - causes:

    • Kidney diseases: Impair potassium excretion.

    • Diarrhea: Loss of potassium-rich fluids.

    • Diuretics: Some diuretics increase potassium excretion.

  • Hypokalemia: Low potassium level - leads to:

    • Muscle weakness, failure of the respiratory muscle and heart, affecting overall bodily function.

  • Hyperkalemia can lead into cardiac arrhythmias, which can be life-threatening.

Acid-Base Balance Refresher
  • Normal plasma pH: 7.38 - 7.42, which is essential for optimal physiological function.

  • Controlled by hydrogen ion concentration, maintaining a narrow range for proper enzyme activity.

  • pH modulates enzyme functionality; abnormal pH affects protein structure and nervous system, disrupting bodily processes.

  • Acidosis: Neurons become less excitable; CNS depression, impairing brain function.

  • Alkalosis: Hyper-excitability, leading to muscle spasms and seizures.

  • pH disturbances are associated with potassium disturbances, as the body attempts to maintain electrical neutrality.

  • Kidneys pump potassium and hydrogen oppositely.

    • Example: Hyperkalemia leads to losing hydrogen ion, or acid, which leads to metabolic alkalosis, illustrating the interconnectedness of electrolyte balance.

Factors Shifting pH
  • Diet (fatty acids, amino acids) can affect pH through metabolic processes.

  • Breathing (carbon dioxide from metabolism) influences pH as carbon dioxide forms carbonic acid.

  • Water (forms carbonic acid) contributes to pH balance but can also lead to imbalances.

  • Production of lactic acid and ketoacidosis lowers pH, leading to acidosis.

Control Mechanisms
  • Buffer system (bicarbonate in extracellular fluid) neutralizes excess acids or bases to maintain pH.

  • Proteins, hemoglobin, phosphates in cells act as buffers to minimize pH changes.

  • Phosphate and ammonia in urine help to excrete excess acids, maintaining pH levels.

  • Respiratory system (ventilation) controls carbon dioxide levels, affecting pH rapidly.

  • Renal system (excretion of hydrogen) regulates pH by excreting or reabsorbing hydrogen ions.

  • Hyperventilation: Washing off carbon dioxide, losing acid (respiratory alkalosis), increasing blood pH.

Buffers and Ventilation
  • Buffers control moderate pH changes by neutralizing excess acids or bases.

  • Cellular proteins, phosphate ions, hemoglobin, and bicarbonate balance pH, maintaining homeostasis.

  • Ventilation rapidly corrects 75% of disturbances but cannot maintain long-term control.

Renal Regulation
  • Receptor-mediated endocytosis reclaims filtered proteins and other molecules.

  • Directly excretes or reabsorbs hydrogen ions, fine-tuning pH levels.

  • Indirectly changes the rate at which bicarb buffer is reabsorbed or excreted, regulating acid-base balance.