Copy of 10. study guide - fluids_lytes.docx

Normal physiology: Fluid balance Patho. change/ predisposing factors (PF) Nursing problems/Assessment findings Interventions Fluid compartments Intracellular -All the fluid in the cells -Makes up about 2/3 of the water in the body Extracellular intravascular (in blood vessels) interstitial (between...

Normal physiology: Fluid balance Patho. change/ predisposing factors (PF) Nursing problems/Assessment findings Interventions Fluid compartments Intracellular -All the fluid in the cells -Makes up about 2/3 of the water in the body Extracellular intravascular (in blood vessels) interstitial (between cells) lymph transcellular (CSF, fluid in various body spaces, joint space) -Small amount in each compartment -Called Third Space if there is a build-up of too much transcellular fluid Movement of fluid between compartments Between cells and interstitium – r/t tonicity or osmolality of extracellular fluid -The fluid carries oxygen, nutrients, & waste products -Moved by osmosis (passive movement that is determined by concentrations in the fluid) -Concentration determines the direction of movement. hypertonic: water pulled out of cells hypotonic: water moves into cells isotonic: no change Between intersitium and intravascular space – determined by: capillary hydrostatic pressure: pushes fluid out of capillary, into tissues -Due to the amount of fluid in the compartment -The more fluid in the compartment, the higher the hydrostatic pressure and it pushes fluid out of the compartment. capillary colloidal osmotic pressure: pulls fluid into capillary -Due to the amount of protein in the fluid of the compartment; proteins draw the fluid in -Colloidal means protein tissue hydrostatic pressure: opposes pushing of fluid out of capillary (pushes fluid out of tissue into capillary) Plasma proteins like albumin are too big, so they stay inside the capillaries and pull fluid in tissue colloidal osmotic pressure: pulls fluid into interstitium -proteins in tissue give the tissue compartment its osmotic power -the pressures are always interacting with each other Some forces work together, other oppose each other -End result is that small amount of extra fluid left in the tissues and is picked up by the lymph system and returned to general circulation by that route Primary functions: maintain vascular volume (blood volume) provide environment for cellular metabolism and other functions to keep cell alive Sources of gain: oral intake, oxidation of nutrients Sources of loss: urine, insensible losses through skin and lungs, stool Regulatory mechanisms: thirst: affects fluid intake ADH: affects fluid output (🡩 water reabsorption in collecting duct of nephron) Pathological change: isotonic increase in extracellular fluid compartment (proportionate losses of sodium and water) PF: Impaired fluid intake inability to obtain fluids (ex: 🡫 mobility, coma, 🡫 access) impaired thirst impaired swallowing Excessive fluid losses GI loss (ex: vomiting, diarrhea, GI suction) renal loss (ex: polyuria, diuretic therapy) skin (ex: 🡩 sweating r/t fever or exercise, burns) third-spacing -If there is a clot in a leg vein, blood can’t get back to the heart so it pools, and capillary hydrostatic pressure goes up, fluid is pushed out from capillaries into tissues and we get edema. Decreased capillary osmotic pressure, so extra fluid ends up in tissues= edema Change is colloidal osmotic pressure like malnourishment and isn’t getting enough protein, so can’t make the plasma proteins like albumin so it can’t draw in the fluid. Where does it go? -Inflammation can change tissue osmotic pressure: capillaries get leaky as part of the inflammation response and some of the plasma proteins leak out into the tissues, so extra osmotic drawing power in the tissues draws the fluid out and we get edema. That’s why edema is one of the cardinal signs of inflammation. -Blood doesn’t have colloidal drawing power and fluid leaks into tissues and that is why the bellies are swollen in starving kids Nursing problem: If Lymph vessel is removed, like a mastectomy, we have now taken away the route for the extra fluid in the interstitial space to get back to the circulation. -2 of the most common problems are fluid volume deficit and fluid volume excess Example of disorder: Isotonic Fluid Volume Deficit -An isotonic decrease of the extracellular fluid compartment -A decrease of the fluid that is outside the cell -This is an isotonic decrease in the fluid; a problem with volume, not a problem with the concentration of that fluid -Na+ is the primary electrolyte in the extracellular fluid, so it controls the concentration of that extracellular fluid -We have lost not just water, but also a proportionate amount of Na+. We have an amount problem, not a concentration problem -When there is a deficit problem, we will get hypovolemia = low blood volume. If less blood = impaired circulation and BP will go down too Assessment findings: -One of the first things we look at is vital signs; BP will drop. -What we see will depend on how much fluid you’ve lost; if you lost a little fluid, you will have orthostatic hypotension or postural. Hypotensive only when you go from laying down to an upright position because when you stand up, the fluid goes down by gravity -BP may be normal when laying down but drops when standing; dizziness, fainting -If fluid deficit is severe, BP will be low even when laying down -When BP goes down, HR goes up as compensatory response to try and bring BP back up -Quality of pulse may be weaker because there’s less blood = thready pulse (faint) due to less blood in the arteries -Body temp will increase because part of the job of circulation is to carry heat from the core of the body out to skin to be released. If less blood, less blood to carry the heat, so we retain the heat and temp goes up -We can check the skin turgor = hydration status and elasticity of the skin; how fast the skin goes down when pinched. Indicates dehydration if it takes a long time for skin to go back down (tenting of the skin) -Weight loss due to fluid loss -People may complain of being thirsty -Urine output is decreased; has concentrated urine because the body is trying to hang on to all the water Deficit: -Replace fluids -First find out why they have a fluid volume deficit. Normal physiology: Fluid balance Patho. change/ predisposing factors (PF) Nursing problems/Assessment findings Interventions Fluid compartments Intracellular Extracellular intravascular (in blood vessels) interstitial (between cells) lymph transcellular (CSF, fluid in various body spaces) Movement of fluid between compartments Between cells and interstitium – r/t tonicity or osmolality of extracellular fluid hypertonic: water pulled out of cells hypotonic: water moves into cells isotonic: no change Between intersitium and intravascular space – determined by: capillary hydrostatic pressure: pushes fluid out of capillary capillary colloidal osmotic pressure: pulls fluid into capillary tissue hydrostatic pressure: opposes pushing of fluid out of capillary (pushes fluid out of tissue into capillary) tissue colloidal osmotic pressure: pulls fluid into interstitium Primary functions: maintain vascular volume provide environment for cellular metabolism Sources of gain: oral intake, oxidation of nutrients Sources of loss: urine, insensible losses through skin and lungs, stool Regulatory mechanisms: thirst: affects fluid intake ADH: affects fluid output (🡩 water reabsorption in collecting duct of nephron) Pathological change: isotonic expansion of extracellular fluid compartment (proportionate gains in water and sodium) PF: 🡫 sodium and water elimination renal failure heart failure (r/t 🡫 renal blood flow) excess corticosteroids (they cause sodium/water retention) Excessive intake of sodium and water dietary administration of medications/IVs that contain 🡩 sodium/water Nursing problem: Example of disorder: Isotonic Fluid Volume Excess/Fluid Expansion/ Fluid Overload -Too much extracellular fluid -Not just gained water, but gained a proportionate amount of Na+ too -Also a fluid volume problem, not fluid concentration problem -If you gain water, but not Na+ too, you would have a concentration problem too because now you have too much water and not enough Na+ Assessment findings: -BP goes up -HR probably won’t change in rate, but may change in quality; full or bounding pulse because there’s a lot of blood in the arteries -Weight will increase due to increased fluid volume -Person will have edema; both peripheral and pulmonary (can tell by listening to lungs; there will be crackles and wet cough, SOB) -Neck vein distension due to too much fluid -If not too severe, we may restrict fluids -Restrict sodium, so you don’t retain water Medication: -If it’s severe and there are signs of edema, then we can give diuretic Normal physiology: Electrolyte balance Patho. change/ predisposing factors (PF) Nursing problems/Assessment findings Interventions Sodium – a cation; most abundant cation in extracellular fluid due to action of the Na+/K+ pump; mostly extracellular. Normal serum level: 135-148 mEq/L ***PRIORITY IS NEURO *** Primary Functions: Regulates extracellular and vascular volume (r/t effect on osmolality or tonicity) Controls the concentration of the fluid -Because you have the most of it; and controls where fluid will move because of hypotonic or hypertonic fluid; also controls how much fluid is inside the cells because of shrinking or swelling. Helps maintain resting membrane potential, and generate action potentials in nerve and muscle tissue -Highly involved in controlling whether you have AP’s in nerve & muscle cells Normal sources of gain: dietary Normal sources of loss: kidneys GI tract (small amount with normal stool) skin (through sweat) Pathological change: loss of serum sodium (<135 mEq/L) PF: Hyponatremia (na in name for sodium) decreased sodium/water loss, accompanied by replacement with sodium-free fluid skin (ex: excessive sweating, burns) GI loss (ex: vomiting, diarrhea, tap water enemas) renal: (ex: aggressive diuretic therapy) Excessive water intake in relation to output (dilutional hyponatremia) psychogenic polydipsia 🡩 intake + impaired elimination (ex: kidney disease, 🡩 ADH levels) Pathological change: Increased serum sodium (>148 mEq/L) PF: Hypernatremia Excess water loss renal (ex: polyuria) GI (ex: watery diarrhea) skin (ex: 🡩 sweating) Decreased water intake (ex: thirst defect, inability to drink) Excessive sodium intake (oral or IV administration, near-drowning in salt water) Nursing problem: Example of disorder: Hyponatremia -Two Ways you can become Hyponatremic: 1. Can lose sodium or gain water (depletion) 2. Dilutional (more common way) “water intoxication” -same sodium as usual -gain water and dilutes the ECF -Somebody who runs marathons and they sweat and lose Na+ and water in the sweat; They lose the water and don’t replace the Na+ Assessment findings: -Low sodium in the blood so you become hypotonic, so water moves into the cell, so cells will swell. This happens first in the brain cells. Symptoms depend on how hyponatremic you are; if mild, person may just have headache, lethargy. If more severe: person may have nausea, confusion, motor weakness -May go into a coma or have seizure if really severe -First assessment should be neuro -When brain cells swell, this affects muscle cells too= resulting in muscle weakness Nursing problem Example of disorder: Hypernatremia Two ways people become Hypernatremic: Taking in too much Na+ More common, to lose water without also losing Na+ -Now it’s a concentration problem -Extracellular fluid is hypertonic, so fluid moves out of cells = intracellular dehydration; cells shrink Assessment findings: -Dry skin, dry mucous membranes -Neuro problems= headache, seizures, coma -Body weight may go down if they lost fluid (more common ways), thirst Identify cause & correct -If sodium was lost, we want to replace it, so we give IV with saline -If person drank too much water, we want to restrict fluid -If already having neuro symptoms like seizures, give diuretic and hypertonic saline IV -Restrict sodium, give fluids Normal physiology: Electrolyte balance Patho. change/ predisposing factors (PF) Nursing problems/Assessment findings Interventions Potassium – a cation; mostly intracellular because Na+/K+ pump is pumping K+into the cell. Normal serum level: 3.5-5.0 mEq/L -2nd most abundant cation in body -Most of K+ is inside the cell ***PRIORITY IS THE HEART*** Primary functions: helps regulate intracellular osmolality Helps maintain resting membrane potential and generate action potentials in nerve and muscle tissue Influences acid-base balance, through compensatory mechanism called “plasma potassium-hydrogen ion exchange” (when serum K 🡫, intracellular K shifts out of cells to 🡩 serum levels 🡪 hydrogen, another cation, must move into cells to replace it 🡪 pH changes. Likewise, changes in pH will affect K levels) Normal sources of gain: dietary Normal sources of loss: mainly through kidneys stool sweat Pathological change: decreased serum levels (<3.5 mEq/L) PF: Inadequate intake Excessive loss renal (ex: diuretic therapy, excessive aldosterone or glucocorticoids) GI (ex: vomiting, diarrhea) skin (ex: heavy sweating, burns) Transcompartmental shifts (from extracellular to intracellular, r/t pH changes, etc.) Pathological change: Decreased serum levels (>5.0 mEq/L) PF: Decreased elimination renal failure aldosterone deficiency K-sparing diuretics Excessive intake (oral or IV) Transcompartmental shifts (release of intracellular K r/t burns, crush injuries, extreme exercise, other types of cell damage WATER FOLLOWS SODIUM Nursing problem: Example of disorder: Hypokalemia -If you are hypokalemic, K+ shifts out of the cell through a compensatory mechanism, Plasma Potassium-hydrogen ion exchange, but H+ will go in and pH in extracellular fluid goes up and becomes alkaline because the acid (H+) is moving out of the extracellular space, into the cell. -The opposite can also happen; if pH out of cell becomes too acidic, we can shift some acid into the cell to buffer and K+ will shift out to take its place. Assessment findings: Alkalosis is a symptom because when you’re hypokalemic, K+ will shift out of the cell to compensate for blood K+, but H+ shifts in, and pH in extracellular fluid will increase and you become alkaline -When ECF is hypokalemic, more K+ will diffuse out of the cell than normal, so the electrical charge becomes more – on the inside than normal, and more Na+ will have to enter the cell to depolarize it, so it becomes harder to generate an AP because you have to wait for more Na+ to get into the cell before it depolarizes. -If it’s harder to generate AP in smooth muscle in GI tract, you will get constipated, due to the decrease in peristalsis movement, and abdominal distention -Nausea -In skeletal muscle, depending on the degree, we see muscle weakness, get tired, muscle cramps -Heart muscle will be harder to generate AP, arrhythmia and CO drops (highest priority to check for) -Interferes with activity of antidiuretic hormone (ADH), so results in an increase in urine output (polyuria). When you’re hypokalemic, kidneys save K+ and dumps out Na+ and water follows so you can’t retain water Nursing problem: -Too much K+ in the extracellular fluid Example of disorder: Hyperkalemia -Too much K+ in the extracellular fluid, so less K+ will leave the cell, so cell is not as negative as usual, so less Na+ has to enter to depolarize it, so it becomes easier to generate an AP. Assessment findings: -Paresthesia, numbness and tingling due to the nerve endings firing out of control. -Diarrhea because of the APs being generated in the smooth muscle of the GI Tract, so there is an increase in peristalsis -There may be cardiac dysrhymias If it’s very severe: -We can lose our concentration gradient; There may be as much K+ on the outside as on the inside; K+ cannot leave the cell and become negative, so cell may depolarize and not able to repolarize again because K+ can’t leave the cell to make the inside negative, so the heart muscle goes into cardiac arrest Hypokalemia: -Give K+ supplements orally if no dysrhythmia yet and not too severe -May replace via IV (must be careful. We never give IV push, only through IV bag and let it infuse over 10-12 hours because person may become hyperkalemic and can have other problems) Hyperkalemia: Depend on severity: If not too bad, may put patient on low K+ diet -If there is dysrhythmia or paralysis, we would do dialysis to get extra K+ out of the blood. Some medications promote the excretion of K+ in the body Normal physiology: Electrolyte balance Patho. change/ predisposing factors (PF) Nursing problems/Assessment findings Interventions Calcium – one of the major divalent (carries 2 electrical charges) cations in body -Carries 2 electrical charges -Most of the Ca+ in body is in the bones and teeth -Most of the Ca+ not in the bones and teeth is in the cell 0.9% in the cell; 0.1% is outside of the cell (ECF) ***Membrane Stabilizer*** -Looking at Ca+ in the extracellular fluid, not in bones -Half of the Ca in the blood travels attached to plasma protein like albumin -The other half is called free or ionized calcium and it’s when this Ca changes, we see imbalances -If there is a change in how much Ca+ is bound to albumin, that will also change how much is free/ionized and that can lead to an imbalance -Not as directly involved in generating an AP as Na+ and K+, but it will affect how easy it is. -Effect on membrane potential; affects how easy it is to generate ap. Membrane Stabilizer; the more calcium, the more stable the membrane is; hard for Na+ to enter an generate an AP -If Ca+ is not present, it is easier for Na+ to enter and generate an AP Distribution: primarily in bone, remainder mostly intracellular small but vital amount located extracellularly extracellular calcium and phosphorus are reciprocally regulated changes in calcium and magnesium levels also affect one another Normal sources of gain: dietary Normal sources of loss: urine Regulatory mechanisms: mostly through kidneys, influenced by: Parathyroid hormone (maintains normal serum calcium levels) Increased renal reabsorption of calcium enhances activation of vitamin D by kidneys Increased release of calcium from bone Vitamin D (functions to maintain bone mineralization) Increased intestinal absorption of calcium Increased renal reabsorption of calcium Decreased parathyroid hormone (to decrease calcium release from bone) Normal serum levels: 8.5-10.5 mg/dL (approximately half of serum calcium is bound to plasma proteins; however, only ionized calcium participates in cellular functions/activities) Primary functions: Influences membrane potential and permeability Necessary for contraction of all muscle types Pathological change: Decreased serum levels (<8.5 mg/dL) PF: Increased intestinal absorption (ex: decreased vitamin D, malabsorption) Increased ability to mobilize from bone r/t altered parathyroid function abnormal renal loss (ex: renal failure) Decreased protein binding (ex: alkaline pH) Pathological change: Increased serum levels (>10.5 mg/dL) PF: Increased bone resorption (ex: excess parathyroid hormone, prolonged immobility, some cancers) Increased intestinal absorption (ex: excess vitamin D, excess dietary calcium) Nursing problem: Example of disorder: Hypocalcemia -Low Calcium in the blood (membrane not stable) -It will be too easy to generate AP Assessment findings: -Paresthesia- Nerve endings are having APs out of control -Tetany-muscle twitching and spasms -Seizures- AP’s out of control -Laryngospasms- bad bronchospasms in airway due to overactive smooth muscle -Cardiac dysrhythmias: heart muscle APs are going out of control -CATS-Convulsions, Arrhythmias, Tetany, Spasms and Stridor: Airway constriction and causes loud breathing; We see with acute hypocalcemia -If chronically low on calcium, we will see weak bones, osteoporosis, fractures, etc. Nursing problem: Example of disorder: Hypercalcemia -Too much calcium in the blood -Will be too hard to generate AP if there is too much calcium Assessment findings: Acute: -Muscle weakness, flaccid muscles: no reflexes, muscle tone -Stupor- really lethargic, sleepy -Cardiac Dysrhythmias -Constipation due to not having peristalsis in GI tract -Chronic: -Chronically high calcium levels -Kidney Stones because body tries to get rid of extra calcium in the urine and stones form. Hypocalcemia: -If mild/chronic, we give oral calcium supplements and vitamin D because you need vitamin D to absorb calcium -If there are seizures or dysrhythmias, we may give calcium in the IV bag Hypercalcemia: ID the cause and fix it if we can -Medications to excrete Ca -Meds to keep Ca from leaving the bones -If you don’t use bones, they demineralize, and calcium enters blood Acid-Base Balance General concepts pH of body fluids must remain within 7.35-7.45 for body cells to function normally -Acid is normal byproduct in metabolism; body is always making acids -Lungs can only get rid of carbonic acid, kidneys get rid of the rest (every other acid) -When pH starts to drop and blood starts becoming acidic, the lungs jump in right away, increase respirations to get rid of more CO2/Carbonic Acid to try and keep you from getting too far out of normal pH range, but the lungs alone cannot bring pH back to normal. Kidneys don’t kick in as fast; may take a few hours and the kidneys keep going until the pH is back to normal. Alterations in pH can affect: Membrane excitability Function of enzyme systems Structure/function of proteins pH determined by relative hydrogen ion concentration Acid: a molecule that can release a hydrogen ion. The higher the hydrogen ion concentration, the more acidic a solution is, and the lower the pH Base: a molecule that can accept or combine with a hydrogen ion. The lower the hydrogen ion concentration, the more basic or alkaline the solution, and the higher the pH Regulation of pH Acids always being generated as byproducts of cellular metabolism Primary routes for acid excretion Lungs/respiratory system. Carbonic acid (H2CO3) can be excreted by lungs in form of carbon dioxide gas (remember equation: CO2 + H2O <-> H2CO3 <-> H+ + HCO3). -Lungs alone cannot get rid of extra acid. They take longer to start -They work together to get rid of the acids, but it takes a while Kidneys/renal system. All other acids are buffered, then excreted by kidneys. -Lungs kick in right away and start to get rid of acid. Kidneys do take a while so we use the temporary mechanisms in the meantime listed below… Temporary means of preventing large changes in pH until respiratory and renal mechanisms become effective: -While we wait for lungs and kidneys to start getting rid of acid Buffer systems – immediately available to combine with excess acids or bases -If pH starts going in one direction or another, the buffer system will jump in and try to keep pH from dropping or going too high. Example: bicarbonate buffer system (most important/primary buffer system): CO2 + H2O  H2CO3  H+ + HCO3 bicarb and carbonic acid, the 2 components of the system, are in chemical equilibrium in extracellular fluid. if too much acid is present, the bicarb ions take up the hydrogen ions released by the acid and become carbonic acid (a weak acid) 🡪 converted to carbon dioxide and water 🡪 carbon dioxide excreted by lungs -has taken a strong acid and made it into carbonic acid, which is a weak acid and can be converted to CO2 and we can exhale it if blood too alkaline, carbonic acid will dissociate to release hydrogen ions (which balances out the alkalinity) and bicarb (a weak base) which can then be excreted by the kidneys in the urine or hang on to it based on the needs of the body. Other buffer systems include protein buffer system phosphate buffers bone buffers Compartmental shifting of acids. Ex: plasma potassium-hydrogen ion exchange. When excess hydrogen ions are present in extracellular fluid, they move into cells for buffering. Means another cation must leave cell 🡪 potassium shifts out of cell. Arterial blood gases (ABGs) (Arterial Blood Gas) Know values!!! PaCO2 – partial pressure of carbon dioxide dissolved in arterial blood – indicator of respiratory component of acid-base balance Normal: 35-45 mm Hg HCO3 – plasma bicarbonate ion concentration – indicator of renal/metabolic component of acid-base balance Normal: 22-26 mEq/L pH – determined by relative hydrogen ion concentration (relative amounts of acids and bases in body fluids). For pH of blood to be normal, the ratio of bicarbonate ion to carbonic acid must be 20:1. even if actual values of bicarb and carbonic acid are not normal, if the ratio is 20:1, pH will still be normal. Called “compensation”. respiratory system can compensate for metabolic-related imbalances by increasing or decreasing ventilation the renal system can compensate for respiratory-related imbalances by making urine more acidic or more alkaline imbalances may be partially or fully compensated Normal: pH 7.35-7.45 -Ratio must be 20:1 to keep in balance pH Terms Acidosis/alkalosis – refer to clinical conditions that result from changes in pH -Classify them as either metabolic or respiratory; 4 primary acid base imbalances Respiratory vs metabolic Respiratory – r/t altered carbon dioxide/carbonic acid levels due to changes in ventilation Metabolic – r/t altered bicarbonate concentration due to changes in acids/bases other than carbonic acid Assessment findings of acid-base disorders result from: the altered pH itself/signs of the imbalance, plus the compensatory response; if it’s metabolic, the lungs should be trying to fix the problem symptoms of whatever disease/disorder caused the pH imbalance in the first place -For example, if it’s metabolic acidosis, you should assess for signs of depressed membrane excitability Extra Notes: -Free calcium competes for binding sites on albumin with hydrogen. Calcium and Hydrogen are both trying to bind to Albumin. -If a patient is in alkalosis, the amount of hydrogen that binds to albumin will decrease because there isn’t as much hydrogen, so more calcium binds to albumin, so the ionized calcium will decrease. Acidosis: decrease membrane excitability: harder to make action potential fix by: removing acid or save base to neutralize Ph Alkalosis: Increase membrane excitability: easier to make action potential fix by: save more acid or get rid of base to neutralize Ph Compensation: If metabolic imbalance (problem caused by kidney) LUNGS try to compensate by: changing rate of respiration so change how much CO2 is exhaled (CO2=acid, since CO2 + H2O= carbonic acid) -Breathing faster and deeper will get rid of more Co2/Acid -Breathing slower and shallower -> Save Co2acid If respiratory imbalance: (problem caused by lungs) KIDNEY tries to compensate by: Changing how much acids/bases are saved or excreted in urine -> Ph of urine will change Metabolic Acidosis: Harder to generate Ap so stuff like.. (Lungs need to breathe more to compensate) -Stupor -Muscle weakness -Cardiac Dysrythmias also look at what the cause is.. ex: renal failure Metabolic Alkalosis: Easier to generate AP… (Lungs need to breathe less to compensate) -Parasthesias -Tetany -Hyperactive reflexes -Seizures Respiratory Acidosis: Harder to generate Ap… (Kidneys need to get rid of acids or save bases, Ph will drop) -Stuper -Lethargy -Coma -C02 Narcosis Respiratory Alkalosis: Easier to generate Ap…. (Kidneys save more acids so une is alkalne) -Usually happens when people hyperventilate Normal physiology: Acid-base balance Patho. change/ predisposing factors (PF) Nursing problems/Assessment findings Interventions Regulation of pH – normal range: 7.35-7.45 Necessary to maintain normal membrane excitability, enzyme system function, structure and function of proteins, etc. Acids continually generated as byproducts of cellular metabolism Primary routes of acid excretion: lungs: the volatile acid carbonic acid can be excreted in form of carbon dioxide gas kidneys: all other acids are nonvolatile – must be buffered and then excreted by kidneys Buffer systems: prevent large pH changes during time it takes for lung and kidney mechanisms to become effective Bicarbonate buffer system: CO2 + H2O  H2CO3  H+ + HCO3 if pH becomes too alkaline, carbonic acid will dissociate to release hydrogen ions, and bicarb, which can be excreted by kidneys as needed if pH becomes too acidic, bicarb ions will take up hydrogen ions and become carbonic acid, which can be eliminated by lungs as needed Compartmental shifting of acids: plasma potassium-hydrogen ion exchange: when extracellular fluid is too acidic, excess hydrogen ions move into cells to normalize extracellular pH 🡪 another cation must leave cell 🡪 potassium shifts out of cell Pathological change: primary deficit in base/bicarbonate (🡫 in pH <7.35 with bicarb <22 mEq/L) PF: Excess metabolic acids 🡩 production (ex: lactic acidosis, ketoacidosis) impaired kidney function 🡪 🡫 acid excretion drug/chemical toxicities (ex: aspirin, ethylene glycol, methanol) Excessive loss of bicarb impaired kidney function 🡪 🡩 renal loss loss of bicarb-rich intestinal secretions (ex: diarrhea, drainage tubes) Hyperchloremia (since chloride and bicarb are both anions, 🡩 chloride causes 🡫 bicarb) Nursing problem: Example of disorder: Metabolic Acidosis -A primary deficit in bicarb; imbalance between amount of acids and bases -Acidosis directly depresses membrane excitability; As soon as you become acidic, it becomes harder to generate action potentials -Lungs should be trying to compensate by increasing respirations and trying to rid the body of excess acid by exhaling CO2 Assessment findings: -Lethargy, weakness, confusion, stupor, coma, dysrhythmias -If renal failure, we do dialysis -Interventions center around trying to correct the cause Normal physiology: Acid-base balance Patho. change/ predisposing factors (PF) Nursing problems/Assessment findings Interventions Regulation of pH – normal range: 7.35-7.45 Necessary to maintain normal membrane excitability, enzyme system function, structure and function of proteins, etc. Acids continually generated as byproducts of cellular metabolism Primary routes of acid excretion: lungs: the volatile acid carbonic acid can be excreted in form of carbon dioxide gas kidneys: all other acids are nonvolatile – must be buffered and then excreted by kidneys Buffer systems: prevent large pH changes during time it takes for lung and kidney mechanisms to become effective Bicarbonate buffer system: CO2 + H2O  H2CO3  H+ + HCO3 if pH becomes too alkaline, carbonic acid will dissociate to release hydrogen ions, and bicarb, which can be excreted by kidneys as needed if pH becomes too acidic, bicarb ions will take up hydrogen ions and become carbonic acid, which can be eliminated by lungs as needed Compartmental shifting of acids: plasma potassium-hydrogen ion exchange: when extracellular fluid is too acidic, excess hydrogen ions move into cells to normalize extracellular pH 🡪 another cation must leave cell 🡪 potassium shifts out of cell Pathological change: primary excess in base/bicarbonate (🡩 in pH >7.45 with bicarb >26 mEq/L) PF: Excess gain of bicarb/alkali medications/IVs Excess loss of hydrogen ions GI: vomiting, gastric suction, etc 🡪 loss of hydrochloric acids + loss of chloride (remember, levels of chloride and bicarb are reciprocal) renal: 🡫 potassium levels due to diuretic therapy 🡪 kidneys excrete hydrogen while trying to save potassium. Also, hydrogen ions shift from extracellular to intracellular because of plasma potassium-hydrogen ion exchange Nursing problem: Example of disorder: Metabolic Alkalosis -Increased membrane excitability; it will be too easy to generate an AP -Lungs should be trying to compensate by slowing breathing/less to retain more carbonic acid to balance alkalinity; more prone to hypoxia due to slowed breathing rate and less oxygenation Assessment findings: -Paresthesia, tetany, hyperactive reflexes, confusion, dysrhythmias Normal physiology: Acid-base balance Patho. change/ predisposing factors (PF) Nursing problems/Assessment findings Interventions Regulation of pH – normal range: 7.35-7.45 Necessary to maintain normal membrane excitability, enzyme system function, structure and function of proteins, etc. Acids continually generated as byproducts of cellular metabolism Primary routes of acid excretion: lungs: the volatile acid carbonic acid can be excreted in form of carbon dioxide gas kidneys: all other acids are nonvolatile – must be buffered and then excreted by kidneys Buffer systems: prevent large pH changes during time it takes for lung and kidney mechanisms to become effective Bicarbonate buffer system: CO2 + H2O  H2CO3  H+ + HCO3 if pH becomes too alkaline, carbonic acid will dissociate to release hydrogen ions, and bicarb, which can be excreted by kidneys as needed if pH becomes too acidic, bicarb ions will take up hydrogen ions and become carbonic acid, which can be eliminated by lungs as needed Compartmental shifting of acids: plasma potassium-hydrogen ion exchange: when extracellular fluid is too acidic, excess hydrogen ions move into cells to normalize extracellular pH 🡪 another cation must leave cell 🡪 potassium shifts out of cell Pathological change: primary excess of carbonic acid (🡫 in pH <7.35 with PCO2 > 45 mm Hg) PF: conditions that impair alveolar ventilation 🡪 🡩 PCO2 -Usually caused by things that impair gas exchange Depression of respiratory center in medulla (ex: head injury, drug overdose) Lung disease (ex: COPD, pneumonia, ARDS, pulmonary edema) Airway obstruction Chest injury Disorders of respiratory muscle Pathological change: primary deficit of carbonic acid (🡩 in pH > 7.45 with PCO2 < 35 mm Hg) PF: hyperventilation; respiratory rate > that needed to maintain normal PCO2 (ex: anxiety/panic attacks, lung disease/hypoxia, fever) Nursing problem: Example of disorder: Respiratory Acidosis Retaining Co2; signs of CO2 Narcosis; sleepy, lethargic, fall into coma, stupor, hypoxia -Too much carbonic acid due to impaired gas exchange -Kidneys should try to compensate by getting rid of more acid in the urine and saving more bicarb; urine will become more acid -pH may drop a lot due to the kidneys taking longer to kick in to fix the problem Assessment findings: -Hypoxia due to not taking in enough O2 -CO2 narcosis; sleepiness, lethargy, coma -Some degree of hypoxia due to poor gas exchange/not taking in enough oxygen Nursing problem: Example of disorder: Respiratory Alkalosis -Caused by hyperventilation-getting rid of more CO2 than they should be -We see it in anxiety attacks, fevers or pain due to respiratory rate increasing -Kidneys try to compensate for the problem by getting rid of more base in the urine and saving more acids but the causes don’t last too long so we usually don’t see changes in the urine because it takes so long for the kidneys to start working. -Kidneys usually take a couple hours, so if panic attack ends, kidney would not have compensated yet Assessment findings: -Dizziness, tetany, seizures. Respiratory Acidosis: -Improving gas exchange to get rid of carbonic acid Respiratory Alkalosis: Body usually corrects on its own due to short-lived causes such as panic attacks. Steps for Interpreting ABG’s (for acid-base imbalances) Look at pH: does patient have acidosis or alkalosis? Look at pCO2 and HCO3: are they high, low, or normal? If they are high or low, would they make the patient more acidic, or more alkaline? For PCO2 (respiratory): remember that CO2 = acid (just add water to CO2 and you get carbonic acid) If it is Increased = more acid If it is decreased = less acid (more alkaline) For HCO3 (kidney/metabolic): remember that bicarb is a base (alkaline) If it is increased = more alkaline If it is decreased = less alkaline (more acidic) Which could have caused the problem identified in the first step -- the PCO2 or the HCO3? If caused by the PCO2, it is a respiratory problem, since PCO2 is our respiratory indicator If caused by the HCO3, it is a metabolic problem since HCO3 is our metabolic indicator Look at the value you did not choose in the last step as being the cause of the problem: Is it trying to compensate for/correct the acid-base problem? If so, was it successful in bringing the pH back within normal limits? If it brought the pH back to normal, the imbalance is fully compensated If it tried to, but did not succeed, the imbalance is partially compensated If it didn’t even try to bring the pH back to normal, the imbalance in uncompensated