| Question | Answer |
| total body water is 40% ICF & 20% ECF---the 20% ECF includes these systems | 20% TBW broken into 15% intersititial and 5% intravascular |
| total body water | 60% of total body weight |
| water moves mostly by | osmosis and hydrostatic p across pmem |
| movement across capillary wall defined by | starling hypothesis=Net filtration = forces favoring filtration – forces opposing filtration |
| figure 3-1 | osmotic pressures pull water from weaker to stronger concentration |
| alterations in water movement --> edema | accumulation of fluid in interstitium |
| edema caused by - finish from 3-3 | Increase in capillary hydrostatic pressure---
Losses or diminished production of plasma ---decreased capialbumin
Increases in capillary permeability
Lymph obstruction (lymphedema) |
| Thirst perception - water balance | thirst perception regulated by osmolality receptors and baroreceptors----also by ADH secretion |
| Na | Primary ECF cation
Regulates osmotic forces
Roles
Neuromuscular irritability, acid-base balance, and cellular reactions |
| Cl | Primary ECF anion
Provides electroneutrality |
| Na/Cl balance maintained by | Renin-angiotensin-aldosterone system
Aldosterone
Natriuretic peptides
Atrial natriuretic peptide
Brain natriuretic peptide
Urodilantin (kidney) |
| alterations in Na/Cl/Water balance - isotonic alterations | Total body water change with proportional electrolyte change
Isotonic volume depletion
Isotonic volume excess |
| hypertonic alterations | Hypernatremia
Serum sodium >147 mEq/L
Related to sodium gain or water loss
Water movement from the ICF to the ECF
Intracellular dehydration
Manifestations: intracellular dehydration, convulsions, pulmonary edema, hypotension, tachycardia |
| more hypertonic alterations | Water deficit
Dehydration
Pure water deficits
Renal free water clearance
Manifestations
Tachycardia, weak pulse, and postural hypotension
Elevated hematocrit and serum sodium levels |
| even more hypertonic alterations | Hyperchloremia
Occurs with hypernatremia or a bicarbonate deficit
Usually secondary to pathophysiologic processes
Managed by treating underlying disorders |
| hypotonic alterations | Hyponatremia
Serum sodium level <135 mEq/L
Sodium deficits cause plasma hypoosmolality and cellular swelling
Pure sodium deficits
Low intake
Dilutional hyponatremia
Hypoosmolar hyponatremia
Hypertonic hyponatremia |
| more hypotonic alterations | Water excess
Compulsive water drinking
Decreased urine formation
Syndrome of inappropriate ADH (SIADH)
ADH secretion in the absence of hypovolemia or hyperosmolality
Hyponatremia with hypervolemia
Manifestations: cerebral edema, muscle twitchig, HA |
| even more hypotonic alterations | Hypochloremia
Usually the result of hyponatremia or elevated bicarbonate concentration
Develops due to vomiting and the loss of HCl
Occurs in cystic fibrosis |
| wow, more hypotonic alterations | wow - maybe there's not any more |
| K characteristics | Major intracellular cation
Concentration maintained by the Na+,K+ pump
Regulates intracellular electrical neutrality in relation to Na+ and H+
Essential for transmission and conduction of nerve impulses, normal cardiac rhythms, and skeletal/sm contract |
| K levels effects these systems | Changes in pH affect K+ balance
Hydrogen ions accumulate in the ICF during states of acidosis. K+ shifts out to maintain a balance of cations across the membrane.
Aldosterone, insulin, and catecholamines influence serum potassium levels |
| hypokalemia | Potassium balance described by changes in plasma potassium levels
Causes: reduced potassium intake, increased potassium entry, and increased potassium loss
Manifestations
Membrane hyperpolarization causes a decrease in neuromuscular excitability, skele |
| hyperkalemia | Hyperkalemia is rare due to efficient renal excretion
Caused by increased intake, shift of K+ from ICF, decreased renal excretion, insulin deficiency, or cell trauma |
| mild hyperkalemia | Hypopolarized membrane, causing neuromuscular irritability
Tingling of lips and fingers, restlessness, intestinal cramping, and diarrhea |
| severe hyperkalemia | The cell is unable to repolarize, resulting in muscle weakness, loss of muscle tone, flaccid paralysis, cardiac arrest |
| Calcium functions | Most calcium is located in the bone as hydroxyapatite
Necessary for structure of bones and teeth, blood clotting, hormone secretion, and cell receptor function |
| phosphate functions, and relative to Ca | most phosphate (85%) located in the bone
Necessary for high-energy bonds located in creatine phosphate and ATP and acts as an anion buffer
Calcium and phosphate concentrations are rigidly controlled
Ca++ x HPO4– – = K (constant)
If concentration of |
| what 3 hormones regulate Ca & Phosphate? | Parathyroid hormone (PTH)
Increases plasma calcium levels via bone reabsorption
Vitamin D
Fat-soluble steroid; increases calcium absorption from the GI tract
Calcitonin
Decreases plasma calcium levels |
| Hypocalcemia | Decreases the block of Na+ into the cell
Increased neuromuscular excitability (partial depolarization)
Muscle cramps |
| hypercalcemia | Increases the block of Na+ into the cell
Decreased neuromuscular excitability
Muscle weakness
Increased bone fractures
Kidney stones
Constipation |
| hyperphospatemia | Osteomalacia (soft bones)
Muscle weakness
Bleeding disorders (platelet impairment)
Anemia
Leukocyte alterations
Antacids bind phosphate |
| hyperphosphatemia - see also hypocalcemia because | because high phosphate levels are related to low Ca levels |
| High K solutions are used | when administering death penalty, causes heart to stop |
| magnesium characteristics | Intracellular cation
Plasma concentration is 1.8 to 2.4 mEq/L
Acts as a co-factor in protein and nucleic acid synthesis reactions
Required for ATPase activity
Decreases acetylcholine release at the neuromuscular junction |
| hypomagnesmia | Associated with hypocalcemia and hypokalemia
Neuromuscular irritability
Tetany
Convulsions
Hyperactive reflexes |
| hypermagnesemia | Skeletal muscle depression
Muscle weakness
Hypotension
Respiratory depression
Lethargy, drowsiness
Bradycardia |
| What is pH | Negative logarithm of the H+ concentration
-----Each number represents a factor of 10. If a solution moves from a pH of 7 to a pH of 6, the H+ ions have increased 10-fold. |
| example of pH log | If a solution moves from a pH of 6 to a pH of 5, the H+ has increased 10 times |
| pH, who regulates acid base and why | Acids are formed as end products of protein, carbohydrate, and fat metabolism
To maintain the body’s normal pH (7.35-7.45) the H+ must be neutralized or excreted
Bones, lungs, and kidneys are major organs involved in regulation of acid-base balance |
| pH how do body acids exist? | Volatile
H2CO3 (can be eliminated as CO2 gas)
Nonvolatile
Sulfuric, phosphoric, and other organic acids
Eliminated by the renal tubules with the regulation of HCO3– |
| buffer systems exists as pairs and are | Associate and dissociate very quickly (instantaneous)
Buffer changes occur in response to changes in acid-base status |
| most important plasma buffering systems | carbonic acid/bicarbonate---and HEMOGLOBIN |
| carbonic acid/bicarb - operates where and how | Operates in the lung and the kidney
The greater the partial pressure of carbon dioxide, the more carbonic acid is formed |
| Mechanism of carbonic acid/bicarb buffering | At a pH of 7.4, the ratio of bicarbonate to carbonic acid is 20:1
Bicarbonate and carbonic acid can increase or decrease, but the ratio must be maintained |
| protein buffering | Proteins have negative charges, so they can serve as buffers for H+ |
| renal buffering | Secretion of H+ in the urine and reabsorption of HCO3– |
| Buffering bwo cellular ion exchange | Exchange of K+ for H+ in acidosis and alkalosis (alters serum potassium) |
| acid-base imbalances - overview | Normal arterial blood pH
7.35 to 7.45
Obtained by arterial blood gas (ABG) sampling
Acidosis
Systemic increase in H+ concentration
Alkalosis
Systemic decrease in H+ concentration |
| respiratory acidosis | elevation of pCO2 due to ventilation depression |
| respiratory alkalosis | depression of pCO2 due to alveolar hyperventilation |
| metabolic acidosis | depression of HC03- or an INCREASE in noncarbonic acids |
| metabolic alkalosis | elevation of HC03- usually due to an ex loss of metabolic acids |
| compensation - renal | Alters bicarbonate and H+ levels in response to acidosis or alkalosis
Much slower response
Excretion and/or reabsorption |
| compensation - respiratory | Alters CO2 retention or loss in response to alkalosis or acidosis
Rapid response
Respiratory rate alterations |
| compensation occurs when | When adjustments are made to bicarbonate and carbonic acid in order to maintain the 20:1 ratio and therefore maintain normal pH
The actual values for bicarbonate to carbonic acid ratio are not normal but the normal ratio is achieved |
| correction occurs when | Correction occurs when the values for BOTH components of the buffer pair (carbonic acid and bicarbonate) have also returned to normal levels |
| anion gap | Used cautiously to distinguish different types of metabolic acidosis
By rule, the concentration of anions (–) should equal the concentration of cations (+). Not all normal anions are routinely measured.
Normal anion gap = [Na+ + K+ ]- [Cl– + HCO3– ]= |
| abnormal anion gap | Abnormal anion gap occurs due to an increased level of abnormal unmeasured anion
Examples: DKA—ketones, salicylate poisoning, lactic acidosis—increased lactic acid, renal failure, etc.
As these abnormal anions accumulate, the measured anions have to de |
