The condition in which the hydrogen ion concentration increases above normal (reflected in a pH below 7.35).
Movement of molecules across cell membranes and epithelial membranes against a concentration gradient; requires energy.
Alkalis are bases that accept hydrogen ions in solution.
The condition where the hydrogen ion concentration decreases below normal (reflected in a pH above 7.45).
Severe, generalized edema.
The difference between the sum of two measured anions, chloride and bicarbonate, and the principal measured cation, sodium.
Arterial blood gas (ABG)
A laboratory test used to evaluate acid-base balance and gas exchange.
Atrial natriuretic peptide (ANP)
A hormone released by atrial muscle cells in response to distention from fluid overload.
Base excess (BE)
A calculated value also known as buffer base capacity. Base excess reflects the degree of acid-base imbalance by indicating the status of the body's total buffering capacity.
A heart rate of less than 60 beats per minute.
A space enclosed by a fibrous membrane or fascia.
Loss of water.
The rapid inflow of sodium ions, causing an electrical change in which the inside of a cell becomes positive in relation to the outside.
The process by which solute molecules move from an area of high solute concentration to an area of low solute concentration to become evenly distributed.
The process by which water and dissolved substances (solutes) move from an area of higher hydrostatic pressure to an area of lower hydrostatic pressure.
Abnormal opening or passage between two organs or spaces that are normally separated or an abnormal passage to the outside of the body.
Fluid volume deficit (FVD)
A decrease in intravascular, interstitial, and/or intracellular fluid in the body.
Fluid volume excess (FVE)
Excess extracellular fluid resulting from retention of both water and sodium in the body.
Tissue that produces secretions or synthesizes hormones.
A group of hormones secreted by the adrenal cortex; they regulate carbohydrate levels in the body.
The process of RBC destruction.
The body's tendency to maintain a state of physiologic balance in the presence of constantly changing conditions.
Decreased circulating blood volume.
A condition of very high blood glucose and insufficient insulin that results in accumulation of ketones and fatty acids in the blood; a form of metabolic acidosis.
Deep, rapid respirations associated with compensatory mechanisms.
Difficulty breathing when supine
The process by which water moves across a selectively permeable membrane from an area of lower solute concentration to an area of higher solute concentration.
Will continue until concentration = on both sides.
Partial pressure of carbon dioxide in arterial blood.
Partial pressuer of oxygen in arterial blood.
The serum bicarbonate (HCO3-) reflects the renal regulation of acid-base balance. It is often called the metabolic component of arterial blood gases. The normal HCO3- value is 22 to 26 mEq/L.
High-pitched, harsh inspiratory sound indicative of upper airway obstruction.
Tonic muscular spasms.
The accumulation and sequestration of trapped extra-cellular fluid in an actual or potential body space as a result of disease or injury.
The application of a straightening or pulling force to return or maintain the fractured bones in normal anatomic position.
Acids eliminated from th body as gas.
Body Fluid Composition: Water
60% of total body wt (varies with age gender and body fat) so women have more fat so less water.
Intake and output should be about equal.
average is 2500ml over 24-hr
-urine output about 1500ml+urine used to excrete feces, inesensible water losses, perspiration
Body Fluid Composition: Electrolytes
chemical compounds-can be intact or dissociate into particles.
Electrolytes are substances that dissociate in solution to form charged particles called ions.
Functios: assist with regulation of water blance, regulate and maintain acid-base blance, contribute to enzyme reactions, essential for neuromuscular activity.
positively charged electrolytes (Na, K, Ca, Mg)
Negatively charged electrolytes (HCO3, HPO4, Cl, SO4)
Body Fluid Distribution
classefied by in or outside of cells ICF and ECF
Intracellular fluid (ICF)
found within cells, essention for normal cell fx, provides medium for metabolic processes.
Extracellular fluid (ECF)
located outside of cells and classified further into locations, Interstitial, intravascular, transcellular.
located in spaces between most of the cells of the body
Intravascular fluid (plamsa)
within arteries, veins and capillaries
urine, digestive secretions; perspiration, cerebrospinal, pleural, synovial, intraocular, gonadal and peridcardial fluids.
Overall ICF and ECF identical except some specific electrolytes differ a great deal (see previous pic)
ICF 40% of tbw
total body fluid is 60% of TBW
plasma 5% of TBW-interstitial and transcellular fluid is 15% of TBW, Extracellular fluid is 20% of TBW.
High potassium (K+), magnesium (Mg 2+) and phosphate (PO4 2-) as well as other solutes such as glucose and oxygen.
Sodium (Na+), chloride (Cl-) and bicarbonate (HC)3-) principalones. High sodium concentration in ECF is essential to regulating body fluid volume. Potassium in ECF is low.
Difference between plasma and interstitial fluid
Calcium (Ca2+) total
Phosphate/inorganic phosphorus (PO4 -2)
188.8.131.52 mEq/L (2.5-4.5 mg/dL)
Magnesium (Mg 2+)
1.6-2.6 mg/dL (1.3-2.1 mEq/L
passage of water, oxygen, carbon dioxide and small water soluble molecules but not proteins and other intracellular colloids.
separate plasma from interstitail fluid (squamous epithelial cells). Allow solute molecules (glucose, sodium), dissolved gases, water to cross.
separate transcellular fluid from interstitial fluid and plasma (include mucosa of stomach, intestines, gallbladder; pleural, peritoneal, synovial membranes and tubules of kidney
concentration of a solution= #solutes/kg ofwater (by weight). reported in milliosmoles per kilogram (MOsm/kg).
Osmality of ECF depends mainly on sodium consentration. Serum osmolity can be estimated by doubling the serum sodium concentration (about 142 mEq/L) glucose and urea contribute to osmolality of ECF but not as much as sodium.
Power of solution to draw water across a membrane. Interstitial fluid and intravascular plasm composition about same except higher concentration of proteins in plamsa (esp albumin) exert colloid osmotic pressure (called oncotic pressure) pulling fluid from the interstitial space into the intravascular compartment. OSMOTIC ACTIVITY OF PLASMA PRTOEINS IMPORT TO MAINTAIN BALANCE AND HELP HOLD WATER IN VASCULAR SYSTEM.
Effect a solution's osmotic pressure has on water movement across the cell membrane of cells within that solution.
same concentration of solutes as plasma. (cells placed in isotonci solution will either shrink nor swell. Normal saline (o.9%) NaCl solution is isotonic
Greater concentration of solutes than plasma. if present water is drawn out o the cell causing it to shrink. 3% NaCl is hypertonic
lower solute concentration than plasma so they will swell. 0.45% NaCl is hypotonic.
rupture-may occur if cells in extremely hypotonic solution.
2 types: simple and facilitated. Both are trying to establish equal concentrations of the molecules on both sides of a membrane.
Simple: random movement of particles through solution, ex water, carbon dioxide, oxygen and solutes move between plasma and interstitial space through capillary membrane. water and solutes move into the cell by protein channels or dissolving in the lipid cell membrane.
Facilitatied diffusion(carrier-mediated diffusion)-allows large water-soluble molecules (glucose and amino acids) to diffuse across cell membranes.
influenced by # of factors: concentration of solute, availability of carrier proteins.
The process by which water and dissolved substances (solutes) move from an area of higher hydrostatic pressure to an area of lower hydrostatic pressure.
Usually across capillary membranes.
Occurs in the glomerulus of the kidneys and arterial end of capillaries.
Created by pumping action of the heart and gravity against the capillary wall. Hydrostatic pressure within the arterial end of the capillary pushes water into the interstitial space. At the venous end of the capillary, the osmotic force of plasma proteins draws fluid back into the capillary.
Allows molecules to move across cell membranes and epithelial membranes against a concentration gradient. ATP and carrier mechanisms is needed. Sodium potassium pump is important example. High concentrations of potassium in intracellular fluids and sodium in extracellular fluids are maintained because cells actively transport potassium from interstital fluid into intracellular fluid.
Body Fluid Regulation
several regulatory mechanisms to balnce fluid intake and excretion: thirst, kidneys, renin-angiotensin-aldosterone mechanism, antidiuretic hormone, and atrial natriuretic peptide.
Primary regulator of water intake.
Thirst center-hypothalamus, stimulated when blood volume drops. Very effective regulating extracellular sodium levels.
Incrased Na in ECF increases serum osmolality which stimulates thirst center.
Fluid intake reduces the Na concentration of ECF and lowers serum osmolality. If serum sodium drups then thirst center inhibited.
Thirst mechanism declines with aging so older adults more vulnerable to dehydration and hyperosmolality. Pts with altered LOC or unable to respond to thrist (intubated, artificially fed) also at risk.
Primary responsible for regulating fluid volume and electrolyte balance by controlling excretion of water and electrolytes.
Adults: 170 L of plasma filtered throug glomeruli daily. About 99% glomerular filtrate reabsorbed only about 1500mL of urine is produced over 24-hr period.
Helps maintain intravascular fluid balance and blood pressure.
↓ blood flow or bp to kidneys stimulates juxtaglomerular cells of nephrons to produce renin (enzyme). Renin converts angiotensionogen (plasma protein) to angiotensin I. Angiotensin I goes to lungs converted to angiotenesin II by ACE. Angiotensin II raises blood pressure. Angiotensin II also stimulates thirst mechanism to promote fluid intake, it acts on kidneys causing them to retain sodium and water. Angiotensin II stimulates the adrenal cortex to release aldosterone. Aldosterone promotes sodium and water retention in the distal nephron of the kidney restoring blood volume.
"Angie tenses the angios"
"Al Do Save Sodium"
Antidiuretic hormone (ADH)
ADH released by posterior pituitary gland
ADH regulates water excretion from kidneys
Osmoreceptors (hypothalamus) respond to increase in serum osmolality and decreases in blood volume stimulating ADH production and release.
ADH makes distal tubules of kidneys more permeable to water thus increasing water reabsorption.
SO urine output falls, blood volume is restored and serum osmolaility drops as water dilutes body fluids.
ADH also increases to stress situations like nausea, pain, surgery, anesthesia, narcotic, nicotine.
ADH is inhibited by alcohol, certain medications (phenytoin) and increased blood volume and decreased serum osmolality.
Atrial natriuretic peptide (ANP)
Hormone released by atrial muscle cells in response to distension from fluid overload.
Affects several body systems: cardio, renal, neural, GI + endocrine.
Primary Fx: oppose renin-angiotensin-aldosterone system by inhibiting renin secretion and bloocking the secretion and sodium-retaining effects of aldosterone.
ANP-promotes sodium wasting and increased urine output.
Fluid Volume Deficit-older adult
Older adults total body water 10% less.
Lean muscle mass lower (body fat % higher)
Sodium and water regulation less efficient
Renal blood flow and glomerular filtration decline.
Kidneys less able to concentrate urine and conserve sodium+water.
Thirst perception decreases.
VERY EASY TO DEHYDRATE
Risk factors: Undetected fevers, self-dcare deficits, confused, depressed, tube fed, bed rest, certain medications (sedative, tranquilizers, diuretics laxatives), no air conditioning, fear of incontinence, physical disabilities (arthritis or stroke), cognitive impairments.
Recognition: may be m ore difficult look for change in mental status, memory or attention, skin turgor not as reliable but do assess over sternum or inner aspect of thigh. Dry oral mucous membraines, increased tongue furrows, subnormal temp, tachycardia and pinched facial expression.
Fluid Volume Deficit
Decrease in intravascular, interstitial and/or intracellular fluid in body.
Can develop slowly or rapidly. Severe fluid loss, hemorrhage, can lead to shock and cardiovascular collapse.
Fluid Volume Deficit-causes
Excessive loss of GI fluids from vomiting, diarrhea, GI suctioning, intestinal fistualas and intestinal drainage. Other causes: diuretics, renal disorders, endocrine disorders, excessive exercise, hot environment, hemorrhage, chronic abuse of laxaties and/or enemas, inability to access fluids, request or swallow fluids, oral trauma, altered thirst mechanisms.
Loss of extracellular fluid volume. Electrolytes often lost with fluid resulting in isotonic fluid volume deficit.
Both water and electrolytes lost the serum sodium levels remain normal but other electrolytes such as potassium may fall. Fluid is drawn into the vascular compartment from the interstiial spaces as body attempts to maintain tissue perfusion.
-regulatory mechanisms are stiumlated to maintain circulation: SNS, thirst mechanism, ADH and aldosterone released.
shift of fluid from vascular space into area not usefuls for normal physiologic processes like abdomen, bowel, pleural or peritoneal space. Fuid may be trapped within soft tissues following trauma or burns. May be in interstitial tissues and unable to support cardio function.
Difficult to assess as may not be reflected in weight or I&O's. Can lead to irreversible shock and multiorgan failure.
Rapid weight loss: 2% of body weight=mild FVD; 5%=moderate FVD; 8% or > = severe FVD.
Sking turgor diminishes skin will remain elevated when pinched.
Postural or orthostatic hypotension. (drop >15 mmHg in systolic BP when changing from lying to standing)
Venous pressure falls=flat neck veins even when pt recumbent.
Tachycardia; pale cool skin (due to vasoconstriction); decreased urine output. Specific gravity of urine increases as water reabsorbed in tubules.
Diagnostic Tests: Serum Electrolytes
Isotonic fluid deficit: Na normal
Water loss only: Na high
Potassium decrease common.
Hemoglobin and hematocirt
Hematocrit often elevated
Urine specific gravity and osmolality
Both increase due to kidneys conserving water.
FVD signs: Mucous Membranes
• Dry; may be sticky
• ↓tongue size, longitudinal furrows ↑
Central venous pressure (CVP)
CVP is mean pressuer in the superior vena cava or right atrium. It is an accurate assesment of fluid volume status.
• Altered mental status
• Anxiety, restlessness
• Diminished alertness/cognition
• Possible coma (severe FVD)
• Diminished skin turgor
• Dry skin
• Pale, cool extremities
• ↓urine output
• Oliguria (severe FVD)
• ↑urine specific gravity
• Orthostatic hypotension (moderate FVD)
• Falling systolic/diastolic pressure (severe FVD)
• Flat neck veins
• ↓venous filling
• ↓pulse volume
• ↓capillary refill
• ↓body temperature (isotonic FVD)
• ↑body temperature (dehydration)
• Weight loss
• 2-5% mild FVD
• 6-9% moderate FVD
• > 10% severe FVD
Mild: Oral rehydration safest. Adults=1500mL/day or 20mL/kg of IBW. replace gradually.
More severe with electrolyte loss: carb/electrolyte solution (sports drink, ginger aile, pedialyte or rehydralyte.
Severe or unable to ingest fluids: IV Therapy with isotonic solutions, hypotonic solutions, hypertonic solutions.
Isotonic electrolyte solutions
0.9% NaCl or Lactated Ringer's solution. Used to expand plasma volume in hypotensive pts or replace abnormal losses. Lactated Ringer preferred to hep prevent acid-base imbalances.
5% dextros in 0.45% saline (D5, 1/2; NS) or 0.45% NaCl (o1/2 normal saline or 1/2NS) provide water for total body water deficits. D5W (isotonic in bag) but becomes hypotonic.
0.45% NaCl with or without added electrolytes. 5% dextrose in 0.45% sodium chloride (D5 1/2NS).
Assess/Diagnoses and Interventions
Assess: I&O; fluid balance. Acute: hourly I&O.
Urine output of < 30mL/hour REPORT. IS inadequate renal perfusion and increased risk for acute renal failure and inadequate tissue perfusion.
Vital signs, CVP, peripheral pulse volume=q4hrs. Hypotension, tachycardia, low CVP and weak easily obliterated peripheral pulses indicate hypovolemia.
Weigh daily (standard conditions).
Assess/Diagnoses and Interventions
-Administer and monitor intake fluids, id beverage preferences. Oral replacement preferred.
-Administer IV as prescribed with infusion pump. Monitor for indicators of fluid overload if rapid fluid replacemtn is ordered: dyspnea, tachypnea, tachycardia, increased CVP, jugular vein distention, edema. Rapid may lead to hypervolemia yielding pulmonary edema and cardiac failure.
-Monitor lab valuers: electrolytes, serum osmolality, BUN, hematocrit.
Assess/Diagnoses and Interventions: Inneffective Tissue Perfusion
-LOC changes: restless, anxious, confused, agitated may indicate inadequate cerebral blood flow and cirulatory collapes
-Monitor serum creatinine, BUN, cardiac enzymes-report elevated to physician. Elevate levles may be impaired renal function or cardiac perfusion related to cirulatory failure.
-Tun Q 2 hrs. good skin care, monitor skin, keep clen, dry, moisturized.
Risk for Injury-dizzy, loss of balance
-teach pt and family how to reduce orthostatic hypotension: moving in stages, avoid prolonged standing, rest in recliner rather than bed, use assistive devices.
FVD community-based care
=imp 1500mL/day +extra to replace perspiration, fever or diarrhea
-manifestations of imbalance
-prevention: dont exercise during heat, more water during heat, sm volume intake if vomiting, reduce caffience, fruit juices or bouillon rather than large amts of tap water, alternate sources of fluid (geletain, frozen juices, ice cream.
Fluid Volume excess
Results when both water and sodium are retained in body.
Heart failure, cirrhosis of liver, renal failure, adrenal gland disorders, corticosteroid administration, ,stress conditions causing release of ADH and aldosterone. Excessive intake of sodium, drugs that cause Na retention, administering excess IV sodium-contianing IV fluids.
Induced by effects of treatment. p. 198
Peripheral edema, or if severe, anascara (severe generalized edema)
Full bounding pulse
distended neck and peripheral veins
incrased central venous pressure (>11-12cm of water)
dyspnea (labored or difficult breathing)
orthopnea (difficult breathing when supine)
Dyspnea at rest
Tachycardia and hypertension
Reduced oxygen saturation
Moist crackles on auscultation of the lungs, pulmonary edema
INcreased urine output (polyuria)
Ascites (excess fluid in the peritoneal cavity)
Decreased hematocrit and BUN
Altered mental status and anxiety
CHF potential cause and compication
limit sodium and water intake
Serum electrolytes+ osmolality measured but usually normal
Serum hematocrit and hemoglobin-decreased
serum creatinine, BUN and liver enzymes may be ordered to help determine cause of excess
Loop diuretics (promote excretion of Na, Cl, K, H2O-loop of henle): Furosemide (lasix), Ethacrynic Acid (edecrin), Bumetanide (Bumex), Torsemide (Demadex).
Thiazide-type diuretics (promote excretion of Na, Cl, K, H2O-distal tubule): Indapamide (Lozol), Bendroflumethiazide (Naturetin), Chlorothiazide(Diuril), Hydrochlorothiazide (HydroDiuril, Oretic), several others p. 199
Potassium sparing diuretics (excretion Na and water by inhibiting sodium potassium exchange in distal tubule): Spironolactone (Aldactone), Amiloride HCL (Midamor, Triamterene (Dyrenium)
Diuretics used to enhance renal function and tx vascular fluid overload and edema.
Common Side effects: orthostatic hypotension, dehydration, electrolyte imbalnce, hyperglycemia.
Patient teaching about diuretics
Drug increase amt an frequency of urination
take even if feel well
take in am
change position slowly
report dizziness; trouble breathing; swelling face, hands or feet
weigh daily report sudden gains and losses
if drug increases potassium loss eat high in potassium foods: OJ and banans,
no salt substitute if you take potassium sparing.
Fluid Management-may be restricted
Dietary Management-sodium restrictions. (high Na foods: lunch meat, bacon, cheese, dry cereal, canned soup, popcorn, ketchup, pickles, seafood.
Oral care may help with fluid restriction. (brush 2x/day; oral moisturizing q 2-4 hrs)
Report to PCP gain of more than 5lb in a week or less
risk factors: meds, heart failure, acute or chronic renal or endocrine disease; recent illness, changes in diet or meds, recent wt gain, persistent cough, SOB, swelling of feet, ankles, difficulty sleeping when lying down.
Wt; vitals, peripheral pulses, capillary refill; jugular vein distention; edema; lung sounds (crackles or wheezes), dyspnea, coug, sputum; urine output; mental status
Nursing Diagnosis/Interventions: Fluid Volume Excess
Fluid Volume Excess
-assess vitals, heart sounds, volume of peripheral arteries.
Hypervolemia can cause hypertension, bounding peripheral pulses and third heart sound (s3)
-Assess edema-usually dependent portions of body, perioribital edema indicates more generalized edema
-daily wts. wt gain 2.2 lbs=1L of fluid gain
-administer oral fluids-record liquids used
-oral hygiene q 2 hours
-teach pt Na restrictions
-administer diuretics and monitor response. loop or high-ceiling diuretics like furosemide can lead to manifestations of hypovolemia +electrolyte imbalance
-report significant changes in serum electrolytes or osmolality.
Assess urine output hourly. Note output less than 30mL/hour or positive fluid balance on 24-hour total intake and output sheet. CHF and inadequate renal perfusion may result in decreased urine output and fluid retention.
Nursing Diagnosis/Interventions: Risk for Impaired Skin Integrity
-frequen skin assessment, esp pressure areas and bony prominences
-reposition q 2 hours
-egg-crate mattress or alternating pressure mattress, foot cradle, heel protectors, other
Nursing Diagnosis/Interventions: Impaired Gas Exchange
-ausculate lungs-crackles, wheezes (indicate pulmonary congestion and edema; ausculate heart for extra heart sounds. (gallop rhythm (s3) may indicate diastolic overloading of the ventricles secondary to fluid volume excess). http://www.youtube.com/watch?v=D6DSKN3jsKE
-Fowler's position for dypnea or orthopnea. (fowlers increases lung expansion)
-monitor O2 sats (<92%-95%); ABG's for impaired gas exchange (PaO2 < 80mmgHg). administer O2 if indicated-it promotes gas exchange improving tissue oxygenation.
-teach manifestations of exccess fluid, when to contact pcp about meds (when to take, adverse effects); diet restrictions; water restrictions, monitoring wt, ways to decrease dependent edema: position changes, no restrictive clothing, no crossing legs, support hose/stockings, elevation of feet and leggs; protecting edematous skin )no barefoot, good fitting shoes; pillows or recliner to sleep to relieve orthopnea.
-low Na helps body excrette excess Na and water
-body needs less than 1/10 tsp salt /day
-1/3 salt from added; 1/4 from processed food/ rest in water and foods high in Na
-Na used in preservatives, leavegning agents, flavor enhances
-Na in nonprescription drugs (analgesics cough meds, laxatives, antacids) toothpastes, mouthwashes
-low na not sodium free
-desire for salt will decrease
-salt, monosodium glutamate, baking soda and baking powder have Na
-herbs, spices, lemon juice, vinegar and wine instead
-most plentiful electrolyte in ECF
-normal 135-145 mEq/L
-500mg/day sufficient to mt needs; CDC 1500mg most americans have 3500mg/day
-Serum sodium < 135 mEq/L (may not see manifestations until 125 mEq/L
-Causes: diuretics, kidney disorders, adrenal insufficiency, vomiting, diarrhea, gastrointestinal suction, GI tube irrigation with water instead saline, repeated water enemas, excessive sweating, loss of skin surface (burns) and 3rd spacing.
--decrease in serum osmolality, ceslls swell
-Manifestations: early( muscle cramps, weakness, fatigue),
below 120 mEq/L: headache, depression, dulled sensorium, personality changes, irritability, lethargy, hyperreflexia, muscle twitching and tremos.
If very low coma likley
- decreased sodium osmolality, decreased hematocrit and BUN, weight loss, lethargy, stupor, coma, anorexia, nausea, vomiting, diarrhea, hypotension, shock
Serum sodium and osmolality decreased
24-hr urine: evaluate sodium excretion
Differential: Increased: SIADH; Decreased: loss of isotonic fluids-sweating, diarrhea, vomiting, 3rd space fluid accumulation)
-Isotonic Ringer's solution or isotonic saline (0.9% NaCl); cautious Iv 3% or 5 % NaCl in pts with low plasma sodium levels (110-115 mEq/L)
-Loop diuretics with normal or excess ECF volume
-drugs to tx cause of hyponatremia
Fluid and Dietary Management
Mild: increase foods high in Na; fluid restriction
Current manifestations (nausea, vomiting, abdominal discomfort, muscle weakness, headache), duration, precipitating factors (heavy perspiration, vomiting, diarrhea); chronic diseases -heart or renal failure, cirrhosis of liver, endocrine disorders, meds.
Mental status, LOC; vitals (inc Othostatic vitals, peripheral pulses); edema or wt gain.
Nursing Diagnosis/interventions: risk for Imbalanced Fluid Volume
-I&O's, daily wts, 24-hr fluid balance
-infusion pump-hypertonic saline (3% and 5% NaCl) Monitor carefuly for pulmonary and cerebral edema
-teach reasons for restriction and restrictions
Nursing Diagnosis/interventions: Risk for Ineffective Cerebral Tissue Perfusion
-due to fluid shifts there can be increased intracellular fluid volume which can cause brain cells to swell, increasing pressure in cranial vault.
-monitor serum electrolytes, serum osmolality-report abnormals (alert to serum sodium and osmolality levels falling-severe manifestations)
-assess neuro changes: lethargy, altered LOC, confusion, convulsions. mental status and orientation. falling Na levels=less responsive
-assessmuscle strength and tone and deep tendon reflexes. (increasing muscle weakness and decreased deep tendon reflexes=increasing HYPOnatremia
Community Based Care
-causes of Na deficits and prevention
-manifestations and what to report
-importance of regular serum electrolyte monitoring if taking diuretic or low Na diet
-foods and fluid needed to replace Na orally
Older adults increased risk for hyponatremia due to meds
Monitor pts Na containing IV solutions for: hypervolemia-increased BP and CVP, tachypnea, tachycardia, gallop rhythm (S3 and/or S4 heart sounds), SOB, cracles) Hypertonic saline solutions can lead to hypervolemia esp if pt has cardio or renal disease.
-Serum Level greather than 145 mEq/L
-Fluid volume deficit or fluid volume excess often accompany
-also known as hypertonic dehydration
-Thirst is first
-initial lethargy, weakness irritability
-can progress to seizures, coma and death if severe
Serum sodium levels greather than 145 mEq/L
Serum osmolality greather than 295 mOsm/kg
-depends on cause
-correct slowly (over 48hrs) to avoid cerebral edema
-Medications: or or IV water replacement-hypotonic Iv (0.45% NaCl or 5% dextrose in water (which is isotonic when administered but becomes hypotonic); diuretics may be given to increase sodium excretion
ID risk factors
teach pts and caregivers
monitor lab tests
-offer fluids at regular intervals or use alternate route (feeding tube)
-duration of manifestations
precipitating factors (water dprivation, increased water loss from heavy perspiration, temperature, rapid breathing, diarrhea, excess salt intake, diabetes insipidus; meds, perception of thirst
Vital signs, mucous membranes; mental status or LOC; manifestations of fluid volume excess or deficit.
Nursing Diagnoses/Interventions: Risk for Injury
-Monitor +maintain fluid replacement
-Monitor serum sodium levels and osmolality;
***rapid replacement of water can cause increase risk of bleeding or cerebral edema
-Monitor neruologic function (mental status, LOC, headache, nausea, vomiting, hypertension and bradycardia).
-Institute safety precautions (bed low, side rails up/padded, airway at bedside) at risk due to seizures and changes in mental status
-Keep clocks other familiar items to keep oriented to time and place.
-respond to thirst
-if prescribed low Na diet
-use and efects of diuretics
-scheduled monitoring of serum electrolyte levels and reporting manifestations
Manifestations of Sodium Imbalances:Hyponatremia
Plasma sodium < 135 mEq?L
Decreased serum osmolality
Decreased hematocrit and BUN
Muscle cramps, weakness
Lethargy, stupor, coma
Anorexia, nausea, vomiting, diarrhea
Manifestations of Sodium Imbalances:Hypernatremia
Plasma sodium > 145 mEq/L
Increased serum osmolality
Increased hematocrit and BUN
Increased thirst, olguria, increased urine output and specific gravity
Dry skin and mucous membranes, decreased skin turgor, furrowed tongue, dry mouth
Tachycardia, hypotension, vascular collapse
Comparison of the Manifestations of Fluid Imbalance: Deficit
Increased heart rate
Decreased Pulse amplitude
Flat Jugular vein
Loose, poor turgor
Low, concentrated output
High urine specific gravity
Comparison of the Manifestations of Fluid Imbalance: Excess
Increased Heart rate
Increased pulse amplitude
Moist crackles and wheezes
Distended jugular vein
Taut skin turgor
Low or normal urine output
low urine specific gravity
-Normal serum (ECF) postassium level is 3.5-5.0 mEq/L; ICF= 140-150 mEq/L
-Must be replaced daily in diet
-Abnormally low less than 3.5 mEq/L
-Usually due to excess potassium loss (hospitalized pts at risk due to inadequate potassium intake)
You need 40 to 50 mEq/day of potassium
-certain drugs: potassium-wasting diuretics, corticosteroids, amphotericin B. lg doses some antibiotics, hyperaldosteronism, renal losses due to stress, trauma, metabolic acidosis and mg deficit.
-gastrointestinal losses from severe vomiting, gastric suction, diarrhea or ileostomy draininage
-transcellular shifts (ECF to ICF) due to tx of diabetic ketoacidosis with insulin, the use of beta2-adrenergic decongestants and bronchodilators.
Mor pronounced when potassium losses occur acutely
-ECG changes include flattened or inverted Twaves, development of U waves and a depressed ST segment
-Nausea and vomiting, anorexia, decreased bowel sounds, ileus
-decreased cardiac output, dysrhythmias (abnormal rhythms)
-Muscle weakness and leg cramps
-Altered kidney function
-Serum potassium levels
-ABG's. incrased pH (alkalosis) is associated with hypokalemia
-Renal function studies (serum creatinine and BUN)-looking for causes or effects
-ECG-to evaluate effects on cardiac system
-Oral and/or parenteral K supplements
-KCl in IV if NPO
-Dosing: daily maintenance requirement+replacement of losses+whatever needed to fix deficit
-High K diet
Foods high in K: pbananas, oranges, avocados, spinach, potatoes, tomatoes, meat, seafood, mok and yogurt.
-balanced electrolyte solutions(pedialyte, sports drinks) to replace abnormal fluid loses (excess perspiration, vomiting, severe diarrhea)
-Patients at risk: pts anorexia nervosa
-encourage diet high in K
-regular monitoring of K levels
Multisystem Effects: Neurologic
Multisystem Effects: Respiratory
Respiratory arrest with severe hypokalemia
Multisystem Effects: Urinary
Polydipsia (excessive thirst)
Multisystem Effects: Cardiovascular
Increased risk of digitalis toxicity
Cardiac arrest (severe hypokalemia)
Multisystem Effects: Gastrointestinal
Nausea and vomiting
Decreased bowel sounds
Multisystem Effects: Musculoskeletal
Poor muscle tone
-current manifestations including anorexia, nausea, vomiting, abdominal discomfort, muscle weakness or cramping
-duration of manifestations
-precipitating factors: diuretic use, prolonged vomiting or diarrhea; chronic diseases such as diabetes, hyperaldosteronism, Cushing's syndrome; current meds
Mental status; vital signs, orthostatic vitals, apical and peripheral pulses; bowel sounds, abdominal distension; muscle strength and tone.
Nursing Diagnoses/Interventions: Decreased Cardiac Output
-monitor serum potassium levels
-monitor vital signs, including orthostatic vitals and peripheral pulses: as cardiac output falls, pulse becomes weak and thready. Orthostatic hypotension may occur
-monitor pts taking digitalis for toxicity (fatigue, weakness, confusion, dizziness, hypotension, nausea)
-monitor response to antidysrhythmic drugs (hypokalemamay incrase resistance)
-Dilute IV postassium, closely monitor IV flow rate and response to K replacement (too fast can lead to hyperkalemia and cardiac arrest)
Severe hypokalemia can cause life-threatening dysrhythmias
-Use cardiac monitor
-Observe for characteristic ECG changes (ST segment depression, flattened T waves and U waves) report rhythm changes immediately.
Never administer undiluted potassium directly into the vein.
Nursing Diagnoses/Interventions: Activity Intolerence
-monitor skeletal muscle strength and tone (affected by moderate hypokalemaia). Increasing weakness, paresthesias or paralys of muscles or progression of affected muscles to include upper extremities or trunk can indicate further drop
-monitor respiratory rate, depth, and effort; heart rate and rhythm; BP at rest and following activity. Tachypnea, dyspnea, tachycardi, and/or a change in blood pressure may indicate decreasing ability to tolerate activities
-Assist with self care activities. increasing muscle weakness cna lead to fatigue.
Nursing Diagnoses/Interventions: RIsk for Imbalanced Fluid Volume
-maintain accurate I&O's
-monitor bowel sounds and abdominal distension-hypokalemia affects smooth muscl function (slowed peristalsis and paralytic ileus)
-meds, postassium supplements
-use of salt substitutes: use if recommended; avoid of taking K supplement or K-sparing diuretic.
-manifestations of K imbalance
-recommendations for monitoring K levels.
-taking digitalis, teach manifestations of digitalis toxicity
-managing GI disorders that cause potassium loss (vomiting, diarrhea, ileostomy drainage)
-KCl is agent of choice because low chloride often accompanies low potassium
-Oral forms: dilute or dissolve, chill (increase palatability), give with food
-Parenteral forms: NO IV PUSH, do not add to fluids already hanging, infuse rate not to exceed 10mEq/hour, do NOT ADMININSTER undiluted, ass injection site (pain, inflammation) IV site ( change first sign of infiltration), use cardiac monitorif if high or rapid dose administered
-assess for abdominal pain, distension, GI bleeding
-assess for hyperkalemia: weekness, feeling of heaviness in legs, mental confusion, hypotension, cardia dysrhythmias, changes in ECG, increased serum K
- >5 mEq/L
can result from inadequate excretion of K, excessively high intake, shift of K from ICF to ECF
affects neuromuscular and cardiac function
p. 209 for patho
Heart, skeletal and smooth muscles affected
-diarrhea, colic (abdominal cramping), anxiety, paresthesias, irritability, muscle tremors and twitching,
AS LEVELS RISE:
-muscle weakness, progressing to flaccid paralysis, lower extremities affected first progresses to trunk and upper extremities. heart rate may be slow (bradycardia) and irregular.
Pathophysiologic Indicators and Manifestations of Hyperkalemia
-Na level > 14 mEq/L
-increased serum osmolality
-increased hematocrit and BUN
-decreased urine output
-increased urine specific gravity
-Dry skin, dry mucous membranes
-increased tongue furrows
Hyperosmolality of ECF=dehydration of brain neurons
Decreased vascular volume
-pulse weak and thready
Serum electrolytes: K level > 5.0 mEq/L; low Ca and Na
ABG's to see if acidosis present
ECG obtained to see effect on cardiac conduction and rhythm.
Goal: lower K, stabilize conduction system of heart
Moderate to severe: calcium gluconate IV (effects last only 1 hr)
To lower K, regular insulin and 50g of glucose administered (shift K out of ECF); sometimes beta2-agonist like albuterol given by nebulizer to temp push K into cells. Na bicarb may be given to treat acidosis.
-Kayexalate used to remove K from the body (oral or rectal)
-if renal fx normal diuretics such as furosemide to promote K excretion
-if renal fx limited peritoneal dialysis or hemodialysis may be implemented
-Greatest risk: those taking K supplements, using potassium-sparing diuretics or salt substitutes and experienceing renal failure; athletes participating in competition sports or who use anabolic steroids, muscle-buiding compounds or energy drinks.
Current manifestations, including numbness and tingling, nausea and vomiting, abdominal cramping, muscle weakness, palpitations; duration, precipitating factors (salt substitutees, K supplements, reduced urine output, chronic diseases such as renal failure or endocrine disorders; current meds.
Apical and peripheral pulses
muscle strength in upper an dlower extremities
Nursing Diagnoses/Interventions: Risk for Decreased Cardiac Output
-closely monitor the reponse to IV calcium gluconate esp if taking digitalis since it increases risk of digitalis toxicity.
monitor ECG for development of peaked, narrow Twaves, prolongation of the PR interval, depression of the ST segment widened QRS interval and loss of the P wave Notify physician of changes. Progressive ECG changes from a peaked T wave to losso fthe P wave and widening of the QRS complex indicate an increasing risk of dysrhythmias and cardiac arrest.
Nursing Diagnoses/Interventions: Risk for Activity Intolerance
Neuromuscular activity affected, funciton of cardiac, smooth and skeletal muscles are affected.
-monitor skeletal muscle strenght and tone (increasing weakness, muscle paralysis or progressoion of affected muscles to upper extremities or trunk.
-monitor repiratory rate and depth. assess lung sounds (muscle weakness can impair ventilation) meds like sodium bicarb or sodium polystyrene sulfonate can cause fluid retention and pulmonary edema.
-assist with self-care (muscle weakness can lead to fatigue)
Prevent future episodes. Teaching points:
-recommeneded diet any restrictions including salt substitutes and foods high in K
-meds to be avoided
Most abudant ion.
Adult= 8.5-10.0 mg/dL.
-regulated by parathyroid hormone (PTH), calcitonin, and calcitriol (a metabolite of vitamin D).
< 8.5 mg/dL
-decreasted total body Ca stores
-low levels of extracellular Ca with normal amts of Ca in bone.
-electrolyte imbalances (hypomagnesemia or hyperphasphatemia), alkalosis, malabosrption disorders, and inadequate vitamin D)
-older adults (esp women) after menopause because of reduced estrogen levels
-alcoholics (alcohol reduces intestinal absorption of Ca)
-massive transfusion of banked blood
-drugs that lower serum mg levels
Monitor pts who have had neck surgery for manifestations of hypocalcemia. Check serum Ca levels and document and report changes.
-level < 8.5 mg/dL
-numbness and tingling around the mouth and in the hands and feet.
-muscle spasms of the face and extremities occur
-deep tendon reflexes become hyperactive.
-carpopedal and laryngeal spasms
-positive Chvostek and Trousseau signs
-carpal spasm induced by inflating a bp cuff on upper arm to above systolic bp for 2-5 minutes
-Decreased blood pressure
-Bone pain, fractures (chronic form)
Most serious manifestations: tetany (tonic muscular spasms) and convulsions, tetany can cause bronchial muscle spasms simulating an asthm attack and visceral muscle spasms producing acute abdominal pain.
Serious: airway obstruction, possible respiratory arrest from laryngospasm, prolonged QT inervals, ventricular dysrhythmias, cardiac arrest, heart failure and convulsions,
-Total Serum calcium
-ionized calcium in critically ill patients
-serum albumin, when low total calcium is likely low
-serum mg: hypocalcemia often associated with hypomagnesemia (< 1.6 mg/dL)
-serum phosphate hyperphosphatemia (> 4.5 mg/dL) can lead to
-ECG evaluate effect on heart such as prolonged ST segment. p. 215
-oral or IV calcium
-If severe tx with IV calcium to prevent airway obstruction
-most common calcium chloride (more irritating to veings may cause venous sclerosis if given in peripheral vein) and calcium gluconate.
-IV calcium: necrosis and sloughing of tissue if infiltrate
-rapid administration can lead to bradycardia and possible cardiac arrest.
-may be combined with D or D may be given alone to incrase GI absorption of Ca
-administer 1- 1.5 hrs after meals and at bedtime
-give with full flass of water
-assess IV site (do not administer if danger of leakage into tissues)
-slow IV push (dilute with sterile normal saline) or added to parenteral fluids like NS, latated Ringer or D5W)
-LARGEST vein to administer- centeral line if available
-do not administer with bicarbonate or phosphate
-Monitor ECG if IV Ca pt is taking digitalis due to incrased risk of digitalis toxicity
-frequently monitor serum Ca levels
-can cause constipation, eat high-biber diet and generous fluid intake
Diet high in Ca if chronic hypocalcemia
-dairy, canned salmon, broccoli, spiniach, tofu
-age associated with total body calcium deficit
-low Ca places at increased risk of osteoporosis, fractures and disability
-women higher risk for osteoporosis as they have lower bone density and hormonal influences.
-Teach adequate Ca intake
-weight-bearing exercise helps with bone density
-regular aerobic and weight-training
-bone density screening for older women
current manifestations, numbness and tingling around mouth and hands and feet, abdominal pain, SOB; acute or chronic diseases such as pancreatitis, iver or kidney disease; current meds.
deep tendon reflexes
presence of convulsions
Nursing Diagnoses/Interventions: Risk for Injury
At risk for: laryngospasm, cardiac dysrhythmias, and
convulsions. If administered too quickly can cause injury to subcutaneous tissues.
-Frequent monitor of airway and respiratory status. report respiratory stridor (high pitched, harsh inspiratory sound indicative of upper airway obstruction) or incrased respiratory rate or effortt to the physician. May indicate laryngeal spasm due to tetany.
-Montor cardiovascular status: heart rate and rhythm, BP, peripheral pulses. Hypocalcemia decreases myocardial contractility reducing cardiac output and hypotension, can cause bradycardia or ventricular dysrhythmias. If severe Cardiac arrest may occur
-ECG continuous monitor, esp if taking digitalis.
-if pt has tetany provide quiet environment and seizure precaustiosn (raise bed rails, keep airway at bedside) quite reduces CNS stimuli reducing risk of convulsions.
Laryngeal spasm is a respiratory emergency requiring immediate intervention tomaintain ventilation and gas exchange.
Discuss risk factors
Teach about meds including calcium supplements
Teach about foods high in calcium and vitamin D if recommended.
Discuss what to report to PCP
Stress importance of follow-up care on schedule
serum calcium > 10.0 mg/dL
Incrased resorption of Ca from bones
-hyperparathyroidsm-excess PTH produced causing CA release from bones and Increased CA absorption intestines, retention of CA by kidneys.
-malignancies-common complication of.
-prolonged immobility and lack of wt bearing
-self-limiting hypercalcemia may follow successful kidney transplant
-altered PTH in chronic renal failure
-increase intestinal absorpition
-some drugs0thiazide diuretics and lithium
Effects of hypercalcemia
-decreases neuromuscular excitability
-leads to muscle weaknes and dpressed deep tendon reflexes
-gastrointestinal motility reduced
-in hear CA effect similar to digitalis: strengthening contractions and reducing the heart rate
-conduction system of the heart affected-leads to bradycardia and heart blocks
-kidneys ability to concentrate urine impaired (excess Na and water loss, increased thirst)
-Extremely high affects mental status: range from personality changes to confusion, impaired memory and acute psychoses
Manifestations of hypercalcemia
-muscle weakness and fatigue
-behavior or personality changes
Complications of hypercalcemia
-Peptic ulcer disease (due to increased gastric acid secretion)
-Pancreatitis (Ca deposits in pancreatic ducts)
-hypercalcemic crisis-acute increase in serum clacium level which can lead to cardiac arrest.
-Serum PTH (to id or r/o hyperparathyroidsm as cause of hypercalcemia)
-ECG: shortened QT interval; shortened and depressed ST segment, widened T wave; Bradycardia or heart block may be id'd
-Bone density scan-monitor bone resorption and tx effects
-IV with loop diuretic (lasix) to promote elimination of Ca
-Calcitonin-promotes uptake of Ca into bones
-bisphosphonates to tx if related to malignzncies
-Emergency-rapid IV admin of sodium phosphate or potassium phosphate (Ca binds to phosphate decreasing serum Ca levels) dangerous can cause fatal hypocalcemia
-IV plicamysin-inhibit bone resorption
-glucocorticoids to compete with vitamin D
-low calcium diet to decrease GI absorption of CA, inhibit bone resporption and incrase urinary Ca excretion
-Calcitonin-decrease skeletal mobilization of Ca and Phosphorus and increase renal output of both.
IV=isotonic saline to restore vascular volume; promote renal excretion of Ca.
-promote mobility; assist to ambulate ASAP
-generous fluid intake 3-4 qts
-limit milk, milk products, Supplements with CA like antacids
-fluids that increase urine acidity (inhibitin stone formation) like cranberry or prune juice.
Health Hx-current manifestation, weakness, fatique, abdominal discomfort, nausea, vomiting, increased urination and thirst; changes in memory or thinking; duration; risk factors like excess intake CA products, prolonged immobility, malignancy, renal failure, endocrine disorders; current medications.
Mental status, LOC, vitals inc apical; bowel sounds; musle strength upper and lower extremeities; deep tendon reflexes.
Ca stabilizes or sedates neuromuscular transmission:
Hypo-increases neuromuscular excitability, muscle twitching, spasms and possible tetany
Hyper-decreased neuromuscular excitability, muscle weakness, and fatigue.
Nursing Diagnosis and Interventions: Risk for Injury
d/t mental status changes, muscle strength changes, bone losing Ca
-potential digitalis toxicity if used: vision changes, anorexia, heart rate and rhythm changes
-Promotoe fluide intake, encourage prune and cranberry for urine acidity
-caution when turning, positioning, transferring or ambulating due to potential fx
Nursing Diagnosis and Interventions: Risk for Fluid Volume Excess
-lg amts isotonic fluids leads to risk for hypervolemia esp with preexisting cardiac or renal disease (loop diuretics may be used)
-Assess frequently-vitals, respiratory status, heart sounds (looking for increasing pulse rate, dyspnea, adventitious lung sounds and S3 on auscultation of the heart may indicate excess fluid volume and potential heart failure.
-Semi-fowler to fowler position: improves lung expansion and reduces wrk of breathing.
-avoid excess intake Ca rich foods and antacids
-use prescriptions as ordered
-increase fluids to 3-4 quarts, increase intake of acid ash foods (meats, fish, poultry, eggs, cranberries, plums, prunes); increase dietary fiber and fluid intake to prevent constipation
-maintain wt-bearing physical activity
1% Mg is extracellular rest cell and bones
Normal serum concentration=1.6-2.6 mg/dL (1.3-2.1 mEq/L)
get from diet: green vegies, grains, nuts, meats, seafood, excreted by kidneys.
-vital to enzyme reactions, protein and nucleic acid synthesis
-Mg has sedative effect on neuromuscular junction, ↓ acetylcholine release.
-esssential ion for neuromuscular transmission and cardio fx.
-Mg affected by K and Ca
< 1.6 mg/dL
-loss gi fluids, diarrhea, ileostomy, intestinal fistula
-disruption nutrient absorption sm intestine
-deficient nutrient intake
-↑ Gi losses
-↑ renal excretion
-protein-calorie malnutrition or starvation
-meds like loop or thiazide diuretics, aminoglycoside antibiotics, amphotericin B, cyclosprine
-rapid administration of citrated blood
-in conjunction with low K and Ca
-causes ↑ neuromuscular excitability with muscle weaknes and tremors
-CNS-can lead to seizures and changes in mental status
-low intracellular mg in myocardium ↑ risk of cardiac dysrhythmias and sudden death
-↑ risk of digitalis toxidity
-chronic may contribute to hypertension
-severe linked to low serum Ca levels
-Neuro: tremors, hyperreactive reflexes, positive Chvostek's and Trousseau's signs, tetany, paresthesias, seizures
-CNS: confusion, mood changes (apathy, depression, agitation), hallucinations, possible psychoses
-↑ heart rate and ventricular dysrhythmias common (esp with hypokalema or pt taking digitalis
-cardiac arrest and sudden death may occur
Hypo/Hyper Mg compared
-ECG shows prolonged PR interval, widened QRS complex and depression of ST segment with T-wave inversion
-Mg added to IV
-pt eat high mg foods (green leafy vegies, seafood, milk, bananas, citrus fruits and chocolate)
-oral mg supplements (can cause diarrhea so limit use)
-parenteral mg sulfate
-Mg IV or deep Im
-renal fx evaluation before administration
-monitor mg levels
IV route for sever mg, neuro changes or cardiac dysrhythmias present.
-adequate Mg intake
-monitor Mg levels report changes
Nursing Diagnoses and Interventions: Risk for Injury
-monitor serum electrolytes 9often accompaniedy by K and Ca deficiencies
-Monitor GI fx including bowel sounds and abdominal distention since hypomagnesium reduces GI motility
-Cardiac monitoring: report and tx ECG changes and dysrhythmias.
-if on digitalis monitor for toxicity
-assess deep tendon reflexes fx during IV mg and prior to IM doses if tdpressed serm Mg level is high
quiet, dark environment, seizure precautions.
-insturct on diet, supplements
-if alcoholic discuss tx options
> 2.6 mg/dL not as comon
-can develop in renal failure
-elevated serum mg levels interfere with neuromuscular transmission and depress CNS
-affects cardio system-potentially causing hypotension, flushing, sweating and bradydysrhythmias
-with lower levels: nausea and vomiting, hypotension, facial flushing, sweating and feeling of warmth
-higher levels CNS depression-weakness, lethargy, drowsiness, weak or absent deep tendon reflexes
-marked elevation-respiratory depression, coma, compromised cardiac fx (ECG changes, bradycardia, heart block and cardiac arrest)
-ID and Tx
-withold antacids, IV's with Mg or enemas
-In renal failure-do hemodialysis or perioteneal dialys to remove excess MG
-Calcium gluconate administered IV
-pt may need mechanical ventilation
-may need pacemaker
-Prevent and ID
-Monitor for critical effects of hypermagnesemia
-ensure pt safety
Potential nursing diagnoses:
-Decreased Cardiac Output r/t altered mycardial conduction
0Ineffective Breathing Pattern r/t muscle weakness and latered level of conciousness
Risk for Ineffective Health Maintenance r/t to lack of knowledge about use of mg-containing supplements, antacids, laxatives and enemas
85% in bones=primary intracellular anion
14% in intracellular fluid
1%in extracellular fluid
Normal Serum phosphate
-essential to production of ATP
-vital to RBC fx and Ox delivery to tissues; nervous system and muscle fx; metabolism of fats, carbs and protein
-assists in maintaining acid-base balance
=ingested in diet, abosrbed in jejunum, excreted kidnesy
-inverse relationship between phosphate and Ca, when one increases other decreases
-PTH, Calcitonin and vitamin D influence phosphate levels
-either low level ofr shift into intracellular space (most common cause)
-decreased GI absorption
-increased renal excretion
-often iatrogenic (r/t tx)
Meds (IV glucose solutions, al or mg based antacids, anabolic steroids, diuretics)
-hyperventilation and respiratory alkalosis cause phosphate to shift to intracellular space
-diabetic ketoacidosis with excess phosphate loss in urie
-< 2.5 mg/dL
-intention tremor, paresthesias
-lack of coordination,
-bleeding disorders (platelet dysfunction)
-impaired white blood cell function
Severe affects virtually every major organ system:
-CNS:-confusion, irritability, apprehension, weakness, paresthesias, lack of coordination, seizures, coma
-Hematologic: Hemolytic anemia may develop due to lack of ATP in RBC's
Musculoskeletal: decreased ATP-muscle weakness and release of creatinin phosphokinases (CPK); acute rhabdomyolysis (muscle cell breakdown) can develop. Muscle cell destruction can lead to acute renal failure
-cardiovascular: decreased myocardial contractility; decreased oxygenation of heart muscale can cause chest pain and ddysrhytmias
GI: anorexia, dysphagia, nausea, vomiting, decreased bowel sounds, possible ileus due to reduced GI motility
-oral phosphate supplements (Neutra-Phos or Neutra-Phos K may restore in mild to moderate
-IV phosphate (sodium phosphate or potassium phosphate when serum level < 1 mg/dL
-monitor closely at pts at risk (malnourised, receiving IV glucose solutions or total parenteral nutrition or being tx with diuretic or antacids that bind with phosphate.
Nursing diagnosis possibilities
-Imparied Physical Mobility r/t muscle weakness and poor coordination
-Decreased Cardiac Output r/t reduced myocardial contractility
-Risk for Injury r/t muscle weakness and altered mental status
-teach causes, manifestation
-teach avoiding phosphorus-binding antacids unless prescribed
-stress well-balanced diet
-nausea and vomiting
-decreased blood pressure
-may be due to impared phosphate excretion, excess intake or shift from intracellular to extracellular
-acute or chronic renal failure primary cause
-rapid administration of phosphate-containing solutions
-excess vitamin D increases phosphate absorpition
-shift from intra to extracellular during chemo, from sepsis or hypthermia or because of extensive trauma or heat stroke
-disruption of calcium regulating mechanisms (hypoparathyroidism, hyperthyroidism or vitamin D intoxication
-few specific manifestations
-muscle cramps, pain parethesias, tingling around the mouth, muscle spasms, tetany really more r/t hypocalcemia that develops secondary to hyperphophatemia.
-Tx of underlying order
-eliminate phosphate-containing drugs
-restrict organ meats, milk and milk products
-agents that bind with phosphate in the GI tract (ex ca containing antacids) may be prescribed
-if renal fx ok, IV normal saline given to promote renal excretion of phosphate
-dialysis may be needed if pt in renal failure
-monitor lab data fo excess phosphorus and deficit of CA as well as manifestations of hypocalcemia
-discuss risk of r/t using phosphate preparations like laxatives or enemas
-teach use of phosphate-binding preps as ordered
-teach dietary phosphate restrictions
-Homeostasis and optimal cell fx require maintenace of the hydrogen ion (H+) within a narrow range.
prevent major changes in pH by removing or releasing hydrogen ions.
-bicarbonate-carbonic acid buffer system
-phosphate buffer system
Bicarbonate-carbonic acid buffer system
-major chemical regulator of plasma pH; ratio of 20 parts bicarbonate to 1 part carbonic acid maintains normal plasma pH
Carbonic acid=weak acid
Normal serum bicarbonate level
regulates carbonic acid by eliminating or retaining CO2
-acidosis=rate and depth of respiration increase
-Alkalosis=depresses respiratory center and both rate and depth of respiration decrease.
-long-term regulation of acid-base balance
-regulate bicarb levels in extracellular fluid
-acidosis: kidnes excrete H+ and retain bicarbonate
-alkalosis: kidneys retain H+ and excrete bicarb
7.35-7.45 (reflects hydrogen ion (H+) concentration
-partial pressure of CO2 in arterial blood
-is measuring the pressure exerted by dissolved carbon dioxide inthe blood.
-represents respiratory component of of acid-base regulation and balance (regulated by lungs)
>45 mmHg= hypercpania
-used interchangeably with PCO2 (the a means arterial blood was used but venous blood is so rarely used often they just drop the a)
80-100 mm Hg
-partial pressure of oxygen in arterial blood
-pressure exerted by oxygen that is dissolved int he plasma (only about 3%) it is the dissolved oxygen that is available to cells for metabolism.
-most oxygen transported in hemoglobin
-valuable for evaluating respiratory fx but not primary to determining acid-base status)
<80 mm Hg= hypoxemia
-used interchangeably with PO2 (the a means arterial blood was used but venous blood is so rarely used often they just drop the a)
bicarbonate concentration in plasma
-reflects renal regulation of acid-base balance
-often called metabolic component of arterial blood gases
-3 to +3
base excess; a measure of buffering capacity
-also known as buffer base capacity
-measures substances that can accept or comine with a hydrogen ion so basically the amount of acid or base that must be added to a blood sample to achieve a pH of 7.4.
ALWAYS DO IN SYSTEMATIC FASHION
ROME=respiratory opposite, metabolic equale
STEPS TO INTERPRETING ABG'S
1. look at pH
STEPS TO INTERPRETING ABG'S
2. Look at PaCo2
,35 mmHg =hypocapnia; more carbon dioxideis being exhaled than normal
>45 mmHg=hypercapnia carbon dioxide is being retained
STEPS TO INTERPRETING ABG'S
3. evaluate pH-PaCO2 relationship for respiratory problem
acidosis (pH<7.35) and hypercapnia (PaCO2>45mmHg)=RESPIRATORY ACIDOSIS
Alkalosis (pH>7.45) and the hypocapnia (PaCO2<35mmHg)=respiratory alkalosis
STEPS TO INTERPRETING ABG'S
4. Look at bicarbonate
HCO3< 22mEq/L lower than normal
HCO3> 26 mEq/L higher than normal
STEPS TO INTERPRETING ABG'S
5. Evaluate the pH, HCO3 and BE for metabolic problem
Metabolic acidosis= pH <7.35; HCO3- <22 mEq/L and BE < -3mEq/L
Metabolic alkalosis=ph is > 7.45/ HCO3 >26mEq/L and BE is > +3 mEq/L
STEPS TO INTERPRETING ABG'S
6. Look for compensation
-Respiratory acidosis (pH < 7.35, PaCO2 > 45 mmHg), kidneys retain HCO3- so HCO3- is <22 mEq/L
-respiratory alkalosis (pH > 7.45, PaCO2< 35mmHg), kidneys excret HO3- to minimize alkalosis so HCO3- is > 22mEq/L
-Metabolic acidosis (pH < 7.35, HCO3- < 22mEq/L), rate and depth of respirations increase, increasing carbon dioxide elimination so the PACO2 <35mmHG.
-Metabolic alkalosis (pH > 7.45, HCO3- >26 mEq/L), respiration slow, carbon dioxide is retained so PaCO2 is > 45 mmHg.
STEPS TO INTERPRETING ABG'S
7. Evaluate oxygenation
PaO2 < 80 mmHg=hypoxemia; possible hypoventilation
PaO2 > 100 mm Hg=hyperventilation
-simple acid-base more common than mixed
*diabetic ketoacidosis (metabolic acidosis)
*chronic obstructive lung disease (respiratory acidosis
*anxiety-related hyperventilation (respiratory alkalosis
-critically ill pts higher risk for mixed acid-base imbalances
changes occur in other parts of regulatory system to restor a normal pH
low pH < 7.35
low bicarbonate < 22 mEq/L
Respiratory system tries to return pH to normal by INCREASING rate and depth of respirations
CO2 elimination increases and PaCO2 falls < 35mm HG
CRITICAL VALUES: pH < 7.20 HCO3- <10mEq/L
Three basic mechanisms that cause metabolic acidosis
-accumulation of metabolic acids
-excess los of bicarbonate
-increase in chloride levels
Metabolic Acidosis: Common causes
-increased acid production
-ketoacidosis r/t diabetes, starvation, alcoholism
-decreased acid excretion
-increased bicarbonate loss
-diarrhea, ileostomy drainage, intestinal fistula
-biliary or pancreatic fistulas
-sodium chlorid IV solutions
-renal tubular acidosis
-carbonic anhydrase inhibitors
Metabolic Acidosis: Manifestations
-affects many body systems
-bradycardia, weakness, fatigue, headache, general malaise, anorexia, nausea ,vomiting, abdominal pain, LOC declines leads to stupor and coma. Cardiac dysrhythmias develop, cardiac arrest may occur. Skin often warm and flushed. Skeletal problems may occur. Compensatory mechanisms seen. Respirations labored, deep and rapid (Kussmauls respirations.http://www.youtube.com/watch?v=0YJxz-Sxx90)
Pt may complain SOB or dyspnea
-ABG's listed above
-Serum electrolytes: elevated K, possible low Mg, Ca may be unchanged
-ECG-may show changes of both acidosis and hyperkalemia
-Blood glucose and renal fx may be done to id cause
-bicarbonate if pH <7.2 ro reduce acidosis effects on cardiac fx.
-Sodium bicarbonate most common Others: lactate, citrate, acetate solutions. If severe alkanizing solutions are IV, if chronic, oral route used.
as metabolic acidosis is corrected, K shifts back into the intracellular space, can lead to hypokalemia and cardiac dysrythmias. Carefully monitor serum K levels during tx.
Tx diabetic ketoacidos
IV insulin and fluid replacement
Alcoholic ketoacidos tx with saline solutions and glucose. Tx for lactic acidosis from decresed tissue perfusion (d/t shock or cardiac arrest) focus on corrrecting underlying problem and improving tissue perfusion.
stress seeking tx if fatigue, general malaise, anorexia, nausea, abdominal pain occur
Assessment: Health Hx
-precipating factors: diarrhea, ingestion toxin like asprin, methanol, ethylene
-chronic disorders: diabetes, renal failure, cirrhosis of liver, endocrine disorders
APical and peripheral pulses
skin color and temp
abdominal contour and distention
FIrm pressure 2-5 minutes after needle removed for arterial blood measurement, maybe long if pt is getting anticoagulants.
Nursing Diagnosis and interventions: Decreased Cardiac Output
-decreased mycordial contractilitys
-slowed hart rate
increasing risk for dysrhythmias
-Monitor for hypotension, diminished pulse strength, slowed capillary refill may indicate decreased cardiac output and impaired tissue perfusion which increases risk for lactic acidosis
-ECG: monitor for dysrhythmias and changes characteristic of hyperkalemai. Progressive ECG such as widening of QRS-indicate risk of dysrhythmias and cardiac arrest
-monitor lab valuse to ensure effective tx.
Nursing Diagnosis and interventions: Risk for Fluid volume excess
-administering of bicarbonate increases risk for hypernatremia, hyperosmolality, and fluid volume excess (water retention)
-monitor hear and lung sounds, CVP and respiratory status: look for increasing dyspnea, adventitious lung sounds and high CVP reading, third heart sound (s3). report to healthcare provider.
-assess urine output, less than 30/mL/hr: heart failure and inadequare renal perfusion may lead to decreased urin output
-administer prescribed diuretics: loop andhigh-celing diuretics can lead to further electrolyte imbalances, esp hypokalemia
Nursing Diagnosis and interventions:Risk for Injury
-monitor neurologic fx
-familiar items around
-significant others around as much as possible
Teach how to prevent, diet, med management, tx for alcoholics, referral for renal failure if applicable.
bicarbonate HCO3- >26 mEq/L
PaCO2 increases > 45mmHg
tx with alkalinizing solutions like bicarbonate