TEST 1: Fluid & Acid-Base Balance Flashcards
Sodium homeostasis mechanisms
- Renin-Angiotensin Aldosterone System (RASS):
- Antidiuretic Hormone (ADH)
- Atrial Natriuretic Hormone (ANP)
Renin-Angiotensin Aldosterone System as a mechanism for sodium homeostasis
- Renin release: low BP/ blood volume triggers release of renin from the juxtoglomerular cells of the kidney
- Angiotensin II formation: renin converts angiotensin (from liver) into angiotensin I, which is then converted to angiotensin II by the angiotensin-converting enzyme (ACE) in the lungs
- Aldosterone secretion: angiotensin II stimulates adrenal cortex to release aldosterone
- Sodium reabsorption: aldosterone acts on distal tubule and collecting ducts of the kidneys to increase sodium reabsorption and water retention (thus elevating blood pressure and volume)
Anti diuretic hormone as a mechanism for sodium homeostasis
- Released in response to high osmolarity: high plasma osmolarity triggers the release of ADH from the posterior pituitary gland
- Water reabsorption: ADH increases the permeability of collecting ducts in the kidneys to water, which promotes water reabsorption and dilution of the sodium concentration of the blood.
ANP as a mechanism for sodium homeostasis
- Release in response to high blood volume: stretch receptors in the atria of the heart sense increased blood volume and release ANP
- Inhibition of RAAS: ANP inhibits renin, aldosterone, and ADH— promoting the excretion of sodium and water (lowering the BP and pressure)
Potassium homeostasis mechanisms
- Aldosterone
- Insulin
- Acid-Base Balance
- Kidney function
Aldosterone as a mechanism for potassium homeostasis
-Aldosterone promotes excretion of K by the distal tubule and collecting ducts in exchange for sodium reabsorption
-Critical for regulating serum K levels
Insulin as a mechanism for potassium homeostasis
-Insulin facilitates the uptake of K into cells (particularly muscle cells) by activating the sodium-potassium ATP-ase pump
-This lowers extracellular K levels
Acid-Base balance as a mechanism for potassium homeostasis
-Acidosis: hydrogen ions enter cells in exchange for K ions—> hyperkalemia
-Alkalosis: hydrogen ions move out of the cell and K ions enter —> hypokalemia
Kidney function as a mechanism for potassium homeostasis
- Filtration and reabsorption: the kidneys filter K in the glomerulus. Most of the filtered K is reabsorbed in the proximal tubule and loop of Henle. The distule tubule and collecting ducts regulate final excretion of K based on body needs.
- K secretion: K is secreted in exchange for sodium under the influence of aldosterone.
Regulation of NA and K
- Body uses negative feedback mechanisms where deviation from normal levels trigger a response to restore balance.
- Hormones like aldosterone, ADH, and ANP play critical roles in regulation of NA and K
- Adequate dietary intake of NA and K is critical for maintaining balance and the kidneys adjust excretion rates to match intake levels.
Sodium and Potassium homeostasis
-Sodium: primarily regulated by RAAS, ADH, and ANP
-Proper NA balance maintains fluid volume, BP, osmotic balance.
Potassium: mainly controlled by aldosterone, insulin, acid-base balance, and kidneys.
-Proper K balance maintains normal cell function, nerve transmission, and muscle contraction.
3 main fluid compartments
-Intravascular (plasma)
-Interstitial
-Intracellular
Intravascular fluid compartment
(Plasma)
-Includes fluid WITHIN the blood vessels
-Contains a high concentration of proteins (esp albumin) which contribute to oncotic pressure as well as a significant amount of electrolytes
-5% of total body weight
Interstitial Compartment
-The fluid that surrounds the cells IN the tissues, OUTSIDE the blood vessels
-Acts as bridge between the Intravascular compartment and the cells, facilitating nutrient and waste exchange
-Accounts for 15% total body weight
Intracellular compartment
-Fluid WITHIN the cells
-Contains high concentrations of K, phosphate, and proteins
-Accounts from 40% total body weight
Mechanisms of fluid shifts
- Osmosis
- Hydrostatic Pressure
- Oncotic Pressure (colloid osmotic pressure)
Osmosis
-Movement of water across a semipermeable membrane from an area of lower solute concentration to an area of higher solute concentration
-Driven by osmolarity, heavily influenced by electrolytes like NA and K.
Hydrostatic pressure
-Pressure exerted by the fluid within the blood vessels
-Pushes fluid out of the capillaries into the interstitial space.
Oncotic pressure (Colloid osmotic pressure)
-Exerted by plasma proteins (albumin) within the blood vessels
-Pulls fluid into the capillaries from the interstitial space
Patterns of fluid shifts between Intravascular and interstitial compartments
- Capillary hydrostatic pressure: drives fluid out of capillaries into the interstitial space (balanced by—>
- Interstitial hydrostatic pressure: opposes movement of fluid out of the capillaries
- Capillary oncotic pressure: pulls fluid back into the capillaries from the interstitial space
- Interstitial oncotic pressure: pulls fluid out of the capillaries into the interstitial space
Starlings Law of Capillary Forces
-The net movement of fluid is determined by the balance of pressures
-Fluid that moves out of capillaries is usually reabsorbed but any excess is drained by lymphatic system
Pattern of fluid shift between interstitial and intracellular compartments
-Osmotic gradient: drives water movement in and out of the cells.
-If interstitial fluid becomes hypertonic (high solute concentration) water will move out of cells into interstitial space
-If interstitial fluid becomes hypotonic (low solute concentration) water will move into the cells.
Pathological fluid shifts
- Edema
- Dehydration
- Third spacing
Edema
-Accumulation of fluid in the interstitial space
Causes:
-Increased capillary hydrostatic pressure (CHF, venous obstruction)
-Decreased capillary oncotic pressure (low albumin d/t liver disease)
-Increased capillary permeability (inflammation, trauma)
-Lymphatic obstruction
(Lymphedema)
Dehydration
-A deficiency of fluid in the interstitial AND intracellular compartments.
-Typically affects interstitial space first (mild dehydration)
-If it Affects intracellular fluid volume it impairs cell function (severe dehydration)
Third-Spacing
-Fluid shifts from Intravascular compartment to potential spaces (ie peritoneal, pleural)
-Often occurs when severe burns, pancreatitis, or sepsis
Intravascular V. Interstitial V. Intracellular fluid
-Intravascular: fluid within the blood cells (high in protein and electrolytes)
-Interstitial: fluid surrounding cells (acts as intermediary between blood vessels and cells)
-Intracellular: fluid inside cells (rich in potassium and protein)
Principles of fluid balance
- Homeostasis
- Fluid compartments:
-ICF: 40% of body weight, primarily within the cells
-ECF: 20% of body weight, consists of Intravascular fluid (plasma) and interstitial fluid - Osmotic pressure: force that drives water across a cell membrane from
An area of low concentration to high until equilibrium is reached. - Hydrostatic pressure: pressure exerted by a fluid due to its weight and the force of the hearts pumping
- Oncotic pressure: osmotic pressure exerted by large molecules (esp albumin) in the blood. Helps to retain fluid in Intravascular space by attracting water.
Mechanisms regulating fluid balance
1.Renal system
2.Endocrine system
3. Thirst Mechanism
4. Fluid intake and output
How the renal system regulates fluid balance
- Kidneys filter blood, reabsorb needed substances, excrete waste and excess fluids
- GFR: determines the rate at which blood is filters to form urine
- NA reabsorption/ electrolyte balance: key to regulating fluid volume due to osmotic effect of NA
- ADH: increases water reabsorption in the kidneys (reducing urine output and increasing intravascular volume)
How the endocrine system regulates fluid balance
- Renin-Angiontensin-Aldosterone system (RAAS):
Renin: converts angiotensin to angiotensin I
Angiotensin II: causes vasoconstriction and stimulates aldosterone release, increasing NA and water reabsorption
Aldosterone: promotes sodium reabsorption and potassium excretion in the kidneys, increasing fluid volume - ANP: released by atrial cells in response to high blood pressure/ volume, inhibits RAAS, and promotes NA and water excretion
How the thirst mechanism regulates fluid balance
-Regulated by hypothalamus in response to increased plasma osmolarity or decreased blood volume
-Stimulated the desire to drink fluids thereby increasing fluid intake
How fluid intake and output affects regulating fluid balance
- Intake: drinking fluids and eating food
- Output: urine, feces, sweat, insensible loss through respiration
-daily balance is usually regulated to match intake with output
Factors influencing fluid balance
- Electrolyte concentrations
- Plasma proteins
- Blood pressure and volume
- Capillary permeability
- Pathophysiologic conditions
How electrolyte contributions influence fluid balance
-Affect osmotic gradients and fluid distribution
-NA is primary ECF cation that influences fluid volume and distribution
How plasma proteins influence fluid balance
-Albumin and other proteins maintain oncotic pressure, retaining fluid within the vascular compartment
How blood pressure and volume influence fluid balance
-BP affects hydrostatic pressure in the capillaries, influencing fluid movement between compartments
How capillary permeability influences fluid balance
-Changes in permeability can affect fluid exchange rates
-Increased permeability can lead to edema
What pathophysiologic conditions influence fluid balance
- CHF, liver and kidney diseases, and dehydration disrupt normal fluid balance mechanisms
What states and mechanisms affect fluid balance
- Osmolality
- Osmosis
- Osmotic Pressure
- Hydrostatic pressure
- Oncotic pressure
- Effective arterial blood volume (EABV)
- ADH
- RAAS
- Natriuretic hormones
- Tonicity
- Isotonic
- Hypotonic
- Hypertonic
- Diffusion
Osmolality
-Measurement of solute concentration per Kg of solvent
-Reflects the number of osmotically active particles in a solution and affects the distribution of water between compartments
Osmosis
-Movement of water across a semipermeable membrane from an area of low solutes to higher solutes.
-Process aims to equalize solute concentrations on both sides of the membrane
Osmotic pressure
-Force exerted by solutes in a solution that causes movement of water across a semipermeable membrane
-Critical for maintaining fluid balance between compartments
Hydrostatic pressure
-Pressure exerted by a fluid due to its weight and volume
-In the body, it’s the pressure exerted by blood against the walls do blood vessels (driving fluid out of the capillaries into the interstitial space)
Hydrostatic pressure
-Pressure exerted by a fluid due to its weight and volume
-In the body, it’s the pressure exerted by blood against the walls do blood vessels (driving fluid out of the capillaries into the interstitial space)
Oncotic pressure
-Type of osmotic pressure exerted by plasma proteins (albumin) in the blood vessels
-Pulls water into circulation from the interstitial space
Oncotic pressure
-Type of osmotic pressure exerted by plasma proteins (albumin) in the blood vessels
-Pulls water into circulation from the interstitial space
Effective arterial blood volume (EABV)
-Concept that reflects the adequacy of blood supply in arterial circulation to maintain organ perfusion and function
-Influenced by cardiac output, blood volume, and vascular resistance
ADH
-Hormone produced by the hypothalamus and released by the posterior pituitary gland
-Promotes water reabsorption in the collecting ducts of the kidneys, concentrating urine and increasing blood volume
RAAS
-Hormone system that regulates blood pressure and fluid balance
-When activated, renin converts angiotensin to angiotensin I, which is then converted to angiotensin II, leading to aldosterone released and increased Na and water reabsorption
Natriuretic hormones
-Released from the heart in response to high blood pressure/ volume
-They promote sodium and water excretion, reducing blood volume and pressure
Tonicity
-Ability of a solution to cause water movement across a cell membrane
-Is influenced by concentration of solutes that cannot cross a cell membrane
-It affects cell volume and function
Isotonic V. Hypotonic V. Hypertonic
Isotonic: solution with same Osmolality as the ICF
Hypotonic: solution with lower Osmolality then the ICF (causes water to move into cells leading to swelling/ lysis)
Hypertonic: solution with higher Osmolality than the ICF (causes water to move out of cells leading to shrinking/ dehydration)
Diffusion
-Passive movement of solutes from an area of high concentration to love concentration, with the aim of equilibrium.
-does NOT require energy and is driven by the concentration gradient
Purpose and function of hydrostatic pressure
-purpose: Force exerted by a fluid in a closed system (blood within blood vessels)
-Function: pressure drives the movement of water/ solutes OUT of capillaries into interstitial space/ tissues.
-Helps delivery of nutrients and oxygen to cells and removal of waste.
Role in fluid balance:
1. Capillary hydrostatic pressure: highest at the arterial and of capillaries, which promotes filtering fluid out of capillary and into interstitial space.
2. Venous end: at the venous end of capillaries pressure is lower allowing for reabsorption of fluid back into capillaries.
-Increased HP: caused by HTN, Fluid overload, obstruction—> leads to increased filtration of fluid out of capillaries (potential edema)
-Decreased HP: caused by hypovolemia or dehydration—> leads to reduced filtration and inadequate tissue perfusion
Starlings Law of Capillary Forces
-Hydrostatic and oncotic pressures work together to regular fluid exchange between the capillaries and interstitial space
-Arterial end of capillaries: hydrostatic pressure is greater than oncotic, promoting fluid filtration INTO the interstitial space.
Venous end of capillaries: oncotic pressure is higher than hydrostatic, encouraging fluid reabsorption into the capillaries.
Pathophysiologic conditions affecting pressure
-Edema:
-increased hydrostatic pressure (CHF)
-decreased oncotic pressure (low levels of albumin)
-increased capillary permeability
-Dehydration:
-decreased hydrostatic pressure (low blood volume— need to activate RAAS to increase hydrostatic pressure)
Effects of aging on body fluid distribution
- Decreased total body water content (less lean muscle mass and more adipose tissues)—> results in having a smaller reserve to draw upon when ill or dehydrated, making them more susceptible to fluid imbalance
Effects of aging on body fluid distribution-
Renal changes
- Changes in renal function (decline in GFR and less ability to concentrate urine)—> results in difficulty regulating fluid volume and electrolytes, higher risk of dehydration and electrolyte imbalances
Effect of aging on fluid distribution-
Thirst mechanism altered
- Altered thirst mechanism (diminished thirst sensation + hypothalamic function/ sensitivity of osmoreceptors)
—> results in not feeling thirsty even when you need fluids, increasing risk for dehydration
Effects of aging on fluid distribution—
Hormonal changes
- ADH: altered regulation/ response to ADH, impacting water reabsorption in the kidneys
- Aldosterone/ renin levels: decreased aldosterone and renin may impair sodium and water reabsorption
-These all affect body’s ability to regulate fluid/ electrolyte balance effectively and increase the likelihood of dehydration and fluid overload
Effect of aging on body fluid distribution—loss of skin elasticity/ efficiency
-decreased turgor: Aging skin loses elasticity and becomes less efficient at retaining water (can lead to increased water loss through skin and decreased ability to buffer against changes in hydration status)
Effects of aging on body fluid distribution— cardiovascular changes
-Decreased cardiac output and vascular elasticity—> leads to problems with blood pressure regulation and tissue perfusion, which impacts tissue distribution and increases the risk of fluid retention/ edema.
Effects of aging on body fluid distribution— chronic illness
-Can significantly impact fluid status
-Polypharmacy
-Requires monitoring of fluid/ electrolyte due to complex nature
Effect of aging on body fluid distribution— metabolic rate
-Metabolic rate decreases, leading to lower overall fluid requirements
-Implies that even minor reductions in fluid intake or slight increase in fluid loss can more easily lead to dehydration
Bicarbonate Buffer System
-Components: Carbonic Acid (H2C03) and Bicarbonate Ion (HC03-)
-Is the most important buffer in the ECF (esp the blood)
-When a strong acid (HCL) is added to the blood, bicarb ions neutralize hydrogen ions, forming carbonic acid
-When a strong base is added to the blood (NaOH), carbonic acid dissociates into hydrogen ions and bicarbonate, neutralizing the base.
-These reactions are readily reversible and act quickly to buffer sudden changes in pH
C02 + H20 <—> H2C03 <—> H+ + HC03-
Phosphate buffer system
-Components: Dihydrogen phosphate (H2P04-) and monohydrogen phosphate ion (HP042-)
-primarily ICF/ renal tubule buffer
-When a strong acid is present, monohydrogen phosphate acts to neutralize the acid, forming dihydrogen phosphate.
-When a strong base is present, dihydrogen phosphate donates a hydrogen ion to neutralize the base, forming monohydrogen phosphate.
-phosphate buffer system has a pKa (acidity of a molecule) that is close normal Ph of ICF, making it an effective buffer.
Phosphate buffer system
-Components: Dihydrogen phosphate (H2P04-) and monohydrogen phosphate ion (HP042-)
-primarily ICF buffer
Plasma protein buffer
-Components: Albumin + Globulin
-Plasma proteins have both acidic and basic groups and can act as buffers by either picking up or releasing hydrogen ions (amphoteric nature).
-proteins contain amino acids with ionizable side chains that can accept (NH2-amino) or donate (COOH-carboxy) hydrogen ions
-Albumin and plasma proteins bind to excess hydrogen ions by reducing the free hydrogen ion concentration and this stabilizing pH.
Hemoglobin buffer system
-Components: Hemoglobin in RBC’s
-Hemoglobin in RBC’s buffers hydrogen ions produced during the transport of C02 from the tissues to the lungs.
-When C02 enters the RBC’s, it resets with water to form carbonic acid, which dissociates into bicarbonate and hydrogen ions. Hydrogen ions are then buffered by hemoglobin.
-Hemoglobin also buffers hydrogen ions released when O2 binds to hemoglobin, facilitating release of 02 in tissues.
Buffer system summary
-Bicarb buffer: Crucial for ECF, neutralizes both acids and bases and is regulated by resp + renal systems
-Phosphate buffer: Effective in ICF + renal tubules, buffers acids and bases by forming dihydrogen and monohydrogen phosphate.
-Plasma Proteins: amphoteric buffers, bind and release hydrogen ions to stabilize plasma pH.
-Hgb buffer: buffers hydrogen ions in RBC’s, facilitates C02 transport and oxygen release.
-All these work together to maintain normal body pH: 7.35-7.45
Metabolic Acids
- Carbonic Acid
- Lactic Acid
- Sulfuric Acid
- Phosphoric Acid
- Ketone bodies (Acetoacetic acid, beta-hydroxybutyric acid)
Carbonic Acid
-Formed from the hydration of C02 in the blood and tissues, catalyzed by the enzyme carbonic anhydrase.
-Important in buffering pH changes in the blood and regulating body’s acid-base balance.
Lactic Acid
-Produced during anaerobic metabolism when glucose is broken down in the absence of oxygen (ie vigorous exercise or hypoxia)
-Acts as a substrate for gluconeogenesis, contributing to energy production and regulating blood pH.
Sulfuric Acid
-Formed from the metabolism of sulfur containing amino acids (ie cysteine and methionine)
-Helps in protein synthesis and metabolic pathways.
Phosphoric Acid
-Present in metabolic processes that involve energy transfer, such as ATP hydrolysis.
-Act as a key component in energy metabolism (including ATP generation and phosphate transfer reactions)
Ketone Bodies
(Acetoacetic acid, Beta-Hydroxybutyric Acid)
-Produced during the metabolism of fatty acids when carbs are limited (starvation, fasting, uncontrolled DM)
-Serve as an alternate source of energy for tissues (mainly the brain) during periods of reduced glucose availability.
Tricarboxylic Acid Cycle
(AKA Krebs/ Citric Acid Cycle)
-Metabolic pathway that occurs in the mitochondria of eukaryotic cells
-Plays a crucial role in generating ATP and the biosynthesis of precursors for cellular processes
-C02 is produced as a byproduct of the TCA cycle, which is instrumental to the acid base balance in the body
C02 + H20 <—> H2C03 <—> HC03 + H+
Role of Carbon dioxide in Acid-Base Balance
-Byproduct of the TCA cycle: C02 is generated during Krebs cycle (key metabolic pathway in mitochondria that produces energy)
-C02 plays a crucial role in maintaining acid base balance through its conversion to bicarbonate ions and hydrogen ions
Equilibrium Reaction
C02 + H20 <—> H2C03 <—> HC03- + H+
-carbonic acid: formed when C02 reacts with water catalyzed by carbonic anhydrase; quickly dissociates into bicarbonate and hydrogen ions
-bicarbonate and hydrogen ions: bicarb acts as a base accepting protons, while hydrogen ions contribute to acidity.
Carbon dioxide/ bicarbonate equilibrium
-Is a key component of the bicarbonate buffer system (one of body’s primary mechanisms for regulating pH and buffering changes in blood acidity)
-Bicarb acts as a base to neutralize excess hydrogen ions to maintain normal Blood pH (prevents drastic shifts in pH)
-C02 elimination through respiration plays large role in balancing levels of carbonic acid and bicarb in the blood
-Kidneys help regulate bicarb levels but secreting excess hydrogen ions and regenerating bicarb to maintain balance
Clinical Implications of C02- bicarbonate system
-Imbalances in C02- Bicarb system can cause respiratory acidosis (excess C02) or alkalosis (decreased C02)
-imbalances in bicarb buffering system can cause metabolic acidosis (low bicarb) or alkalosis (high bicarb)
-The C02- Bicarb equilibrium is crucial for gas exchange in the lungs (where C02 is eliminated) and bicarb is carried in the bloodstream
-The relationship between C02 and bicarb influences energy production, acid base balance, and metabolism
How the kidneys play a role in maintaining acid bad balance
- Reabsorption of bicarb: kidneys reabsorb filtered bicarb which maintains the body’s buffering capacity and prevents acidity in the blood (impaired reabsorption of of bicarb can lead to metabolic acidosis)
- Renal excretion of hydrogen ions: kidneys excrete hydrogen ions through urine to maintain normal pH (impaired excretion can cause metabolic or respiratory acidosis)
- Excretion of hydrogen as ammonium: kidney converts excess hydrogen ions into ammonium and excretes them through urine (impaired ability to convert to ammonium can cause metabolic acidosis).
Metabolic Acidosis
-Occurs when there is an excess of acid in the body or a loss of bicarb (decreased blood pH)
Effects: Hyperkalemia (kidney less able to excrete in acidosis, altered membrane function), hypocalcemia, disruption of metabolic functions, arrhythmias, CNS symptoms
Metabolic Alkalosis
-Results from an excess of bicarb in the body or a loss of acid (increase in pH)
-Effects: Hypokalemia, arrhythmias, hypocalcemia, impaired O2 delivery d/t changes In the oxygen hemoglobin dissociation curve, renal vasoconstriction
Respiratory Acidosis
-Occurs when there is inadequate C02 elimination, causing an increase in carbonic acid levels (decreased pH)
-Effects: CNS depression, vasodilation, hyperkalemia, impaired respiratory drive
Respiratory Alkalosis
-Results from excessive exhalation of C02, leading to a decrease in carbonic acid levels (increased pH)
-Effects: hyperventilation, decreased cerebral blood flow, decreased ionized calcium, respiratory muscle fatigue
Metabolic Acidosis V Metabolic Alkalosis
Etiology
Acidosis: can result from DKA, lactic acidosis, renal failure, diarrhea
Manifestations: kussmaul respirations, confusion, vomiting, dehydration
Alkalosis: can result from vomiting, excessive bicarb containing antacids, hypokalemia
Manifestations: muscle weakness/ cramps, seizures
Respiratory Acidosis V Alkalosis
Manifestations
Acidosis: can result from conditions that impair ability to eliminate C02 (COPD, resp paralysis, inadequate ventilation)
Manifestations: headache, confusion, rapid shallow breathing, cyanosis, pulmonary HTN
Alkalosis: can by caused by hyperventilation (excessive elimination of C02)
Manifestations: dizziness, anxiety, palpitations tachycardia
