Ch 26) Fluid, Electrolyte, and Acid/Base Balance Flashcards
Fluid Compartments
- Two Main Fluid Compartments
- Intercellular Fluid (ICF) compartment
- 25 L (about 40% of the body weight)
- Extracellular Fluid (EFC) compartment
- Outside the cells
- 15 L (about 20% of Body weight)
- Plasma) 3L
- Intersitital Fluid) 12 L found in spaces between cells
- Lymph, CSF, Eye Humors, synovial Fluid, Serous Fluid, Gastrointestinal secretions.
Compasion of Extracellular and Intracellular Fluids
- ECF
- All similar to Plasma (Plasma has a higher protein content/ lower Cl- Content compared to ECF)
- Major cation) Na+
- Major anion) Cl-
- ICF)
- Low Na+ and Cl-
- Major Cation: K+
- Major anion: HPO42-
- Cells have more soluable protiens than plasma (ICF greatest protein content)
Fluid Movment Among Compartments
- Osmotic and Hydrostatic Pressures regulate continuious exchange and mixing of fluide
- Water moves freely along somotic gradients
- Changes in Solute concentration leads to net flow
- ECF Osmolity High > Water Leaves the cell
- Low ECF Osmoliity > Water enters the cell
- Rise In Osmality
- Stimulates thirst, ADH release
- Decrease in Osmoality
- Thirst inhibition, ADH inhibition
Regulation of Water Intake
- Thirst Mechanism driving force for water intake
- Hypothalmic Thirst Center) primary stimilus
- Osmoreceptors detect EFC osmality increase, Dry mouth,
- Baroreceptors) Detect decreased blood volume or pressure (activate thirst centernter and angiotensin II)
- Drinking water = Inhibition of thirst center
- Relif of Dry mouth
- Activaion of Stomach and intestinal stretch receptors
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Regulation of Water Output (ADH)
- Water Reabsorption in collecting ducts proportional to ADH release
- Low ADH> Dilute urine and low volume of body fluids
- High ADH > Concentrated Urine and high volume of body fluids because of reabsoprtion of water
- Hypothalamic osmoreceptors sense ECF solute concentration and regulate ADH accordingly
- Other facotrs that trigger ADH
- Large changes in blood volume or pressure
- Vomiting, Diarrhea, Servere blood loss
Dehydration
- Dehydration) Negative fluid balance
- ECF water loss (hemmorage, severe burns, prolonged vomiting/diarrhea, profuse sweating, water deprivation, ednocrine disurbances)
- Sticky oral mucosa, thrist, dru flushed skin, oliuria
- may lead to weight loss, fever, metal confusion hypovoemic shock
Hypoteonic Hydration
- Cellular Overhydration or water intoxication
- Occurs with renal insufficency or rapid excess water ingestion
- ECF osomality low > Hyponatremia (low ECF Na+ concentration) > net osmosis into tissue cells > swelling of cells > metabolic distrubances > possible death
- Treated with hypertonic saline to reverse osmotic gradients
Edema
- Atypical accumulation of IF in tissues but not the cell
- causes swelling
- Increase of fluid out of blood caused by increaded Capillary Hydrostatic Pressure (HPc) and permiablity
- Hypoproteinemia) down plasma protein levels resulting from protien malnutrition, liver diesease
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Electrolyte Balance
- Salts, acids, bases and some proteins
- Electrolyte Balnce) ususaly refers only to salt
- control fluid movments
- provide minerals essential for excitibality, secretory activity, and memrane permiablity
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Role of Sodium
- Most abundant cation in the ECF
- only cation exerting signifigant osmotic pressure
- Concentration of Na+ in ECF) determines osmolaity of ECF
- influences excitability of nuerons and mucles
- Content of Na+ in body) Determines ECF volume and blood pressure.
- Regulation of Sodium Blance
- No Known receptors that moniter Na+ levels in body fluifs
- Changes in blood pressure or volume trigger neural and hormonal controls to regulate Na+ content
- Aldosterone
- Decreases urinary output; Increases blood volume
- Increases active reabsorption of Na+
- Increases K+ secretion
Regulation of Patassium Blanace
- Impotance of Potassium
- Affects Resting membrane potential (RMP) in nuerons and muscle cells.
- High ECF K+ > Low RMP > leads to depolarization and decresed exitability
- Low ECF K+ > Hyperpolarization and nonresponsiviness
- Hyperkalemi) too much K+
- Hypokalemia) too little K+
- Both disrupt electrical conduction to the heart
- sudden death
- Aldesterone) K+ secretion and Na+ absorption
Regulation of Calcium
- 99% of body’s calcium found in the bones
- Ca2+ in ECF important
- blood clotting, cell membrane permiablity, secretoru activities
- Nueromucular excitability (most important)
- Hypocalcemia) High excitability and muscle tetany
- Hypercalcemia) inhibits nuerons and mucle cells
- may cause heart arrhythmias
- Calcium balance controlled by PTH from parathyroid gland
- PTH promotes increase in calcium levels
Acid-Base Balance
- pH affects all functional proteins and biochemcial reactions
- closley regulated
- Normal pH of body is 7.4
- Alkalosis (alkelemia) arterial pH > 7.4
- Acidosis Acidemia) arterial pH < 7.35
- Most H+ is produced by metabolism
- Loading and transport of CO2 in the blood as HCO3 - liberates h+
- Concantration Hydrogen ions regulated sequentially by
- Chemical buffer system) rapid first line of defense
- Brain stem Repritory centers) change in respritory rate to compensate for acidosis or alkalosis
- 1-3 mins
- Renal Mechanism) strongest but requires hours/ days to effect pH.
Chemical Buffer Systems
- A system of one or more compounds that resists changes in pH when a strong acid or base is added.
- Bind H+ ions when pH drops
- Releases H+ when pH rises
- Water
- strong acids completely dissociate
- Weak acids partialy dissociate; efficent at preventing pH changes
- Strong bases dissociate easialy; pick up H+
- Weak bases less likley to pick up H+
Bicarbonate Buffer System
- Mixture of cabronic acid (H2CO3 / weak acid) and sodium bicarbonate (NaHCO3 / weak base)
- Strong acid added
- HCO3 ties up H+ and frome H2CO3
- Strong Acid + Weak Base > Weak acid + salt
- HCL + NaHCO3 > H2CO3 + NaCl
- increases pH only slightly
- if enough acid is in blood avaible HCO3- will be used up (alkaline reserve) and bicarbionate becomes ineffective
- If Strong Base is added
- H2CO3 dissociates to donate H+
- H+ ties up the base (OH-
- Stong base + Weak acid > Weak Base and Water
- NaOH + H2CO3 > NaHCO3 + H2O
- pH rises only sightly
- H2CO3 supply is almost limitless.
Phosphate/ Protein Buffer Systems
- Phosphate Buffer System
- Salts of H2PO4 (Weak acid) and HPO42- (weak base)
- Imporant in urine and ICF
- Protein Buffer System
- Some amino acid side chains act as weak acids (COOH) or weak bases (-NH2)
- most important buffer in ICF and in Blood Plasma
Physiological Buffering Systems
- Respritory an Renal Systems
- Regulate amount of acid or base in the body
- Acts slower than chemical systems
- More capicicity than chemical systems
Respritory Regulation of H+
- Eliminates CO2 (an acid)
- Reversiable equilibrium equation
- CO2 + H2O <> H2CO3 <>H+ + HCO3-
- Rising plasma H+
- acitvates chemoreceptors
- Increased respritory rate and depth
- More CO2 removed/ H+ conentration is reduced
- Alkolosis Depresses respritory center
- Rate and depth decrease
- H+ concnetration increases
- Respritory impariment causes acid-base imbalance
- Hypoventilation > Respritory acidosis and hyperventilation > respriatory alkalosis
Renal Mechanisms of Acid-Base Balance
- CO2 combines with water in tubular cell. Forms H2CO3
- H2CO3 quickly split into H+ and HCO3-
- H+ secreted into filtrate
- For Each H+ secreted. one HCO3- enters the peritubular capillary
- Secreted H+ recombines with HCO3- in filtrate forming carbonic acid
- H2CO3 dissicoates to release CO2 and H2O
- CO2 diffuses into the tubule cell, where it triggers further H+ secretion.
- To reabsorb bicarbionate kidneys secrete H+
- rate of H+ secretion changes with ECF CO2 levels
- CO2 up in peritubular capilary = Increased rate of H+ secretion
Abnrormalitities of Acid-Base Balance
- All cases of acidoesis and alkalosis can be classed according to cause
- either respritory or metabolic factors
- Respriotry Acidosis and Akalosis
- causes by failure of respritory system to perform pH balancing role
- Indicated by blood PCO2
- Metabolic acidosis and alkalosis
- All abnormalities other than those caused by PCO2 levels in the blood
- Indicated by abnormal HCO3- levels
Respritory Acidosis and Alkalosis
- Most important indicator of adequacy of respritory function is a normal PCO2 level
- normally 35-45 mm Hg
- PCO2 above 45 mm Hg > Respritory Acidosis
- PCO2 below 35 mm Hg > Respritory alkalosis
- result of hyperventilation (CO2 eliminated faster than produced)
Metabolic Acidosis and Alkalosis
- Metabolic acisodis) Low blood pH and low HCO3- levels
- Causes
- Ingestion of too much alchcol (metabolized to acetic acid)
- Excessive loss of HCO3-
- Accumulation of latic acic (excercise or shock), diabetic crisis, starvation and kidney failure
- Metaboic Alkalosis) much less common
- rising blood pH and HCO3- levels
- Causes incude vomiting of acid contents or excess bas intake.
Effects of Acidosis and Alkalosis
- Blood pH below 6.8
- Depression of CNS > Coma > deth
- Blood pH aboce 7.8
- excitation of nervous system > Muscle tetany / Extrme nervousness > Convusions > and death from respritory arrest.
Respritory and Renal Compensations
- If acid-base imbalnce is due to malfunction of physilogical buffer system another system will act to compensate
- Respritoy system attempts to correct metabolic acid-base imbalances
- Kidneys attempt to correct resrpiroty acid-base imbalance
Respritory Compenstation
- Changes in respritory rate and depth are evident when the respritory system is attempting to compensate for acid-base imbalances
- Metabolic acidosis
- high H+ levels stimulate respritory centers
- Rate and Depth of breathing elevated
- blood pH 7.35 and below / HCO3- levels low
- as CO2 is elimintated PCO2 is elimiated
- Metabolic alkalosis
- shallow breathing allows CO2 accumulation in the blood
- Evidence of metabolic alkalosis being compensated by resprirtory mechanism including a high pH / elevated HCO3- levels
- PCO2 levels above 45 mm Hg
Renal Compensation
- Hypoventilation causes elevated PCO2
- respriotry acidosis
- Renal compensation indicated by high PCO2 and HCO3-
- Respritory alkalosis exhibits low PCO2 and high pH
- Renal compensation is indicated by descreasing HCO3- levels.