1 FLUIDS
60 % Extracellular Fluid 20% or 1/3
Intracellular Fluid 40% or 2/3
Arterial Fluid 2%
Venous Fluid 3%
Intravascular 5% or 1/4
Interstitial 15% or 3/4
Transcellular fluid 1-2% ie csf, pericardial, synovial, pleural,lymph system, intraocular
FLUIDS
•Maintain homeostasis •Ensure adequate tissue perfusion •Help maintain body temperature and cell shape •Help transport nutrients, gases and wastes Fluids •60% of an adult’s body weight * 70 Kg adult male: 60% X 70= 42 Liters •Infants = more water •Elderly = less water •More fat = ↓water •More muscle = ↑water •Infants and elderly - prone to fluid imbalance Factors that influence amount of body fluids: 1. age - younger people have higher percentage of body fluid than older people 2. gender - male > women 3. body fats - obese people have less fluids than thin people (fat cells contain little water) Intravascular space - fluid within the blood vessels , contains plasma
- approximately 3L of the average 6L of blood is made up of plasma Interstitial space - contains fluids that surround the cell; about 11-12 liters Transcellular space - contains 1 L of fluid ex. Cerebrospinal, pericardial, synovial, intraocular and digestive secretion Sources of Fluids Fluid Intake 1. Exogenous sources •Fluid intake oral liquids – 1, 300 ml water in food – 1, 000 ml water produced by metabolism – 300 ml
•IVF •Medications •Blood products 2. Endogenous sources •By products of metabolism •secretions Fluid Output Sensible loss
•Urine - 1, 500 ml •Fecal losses – 200 ml Insensible loss
•skin – 600 ml •Lungs – 300 ml
2 Third-space fluid shift/ Third “spacing” - loss of ECF into a space that does not contribute to equilibrium between ICF and ECF - ie ascites, burns, peritonitis, bowel obstruction, massive bleeding
2. Usually occurs across capillary membranes D. Active Transport: molecules move across cell membranes against concentration gradient; requires energy, e.g. Na – K pump Transport Mechanisms
Mechanisms of Body Fluid Movement (i.e. movement of solutes, solvents across different extracellular locations) A. Osmosis: water is mover; water moves from lower concentration to higher concentration 1. Normal Osmolality of ICF and ECF: 275 – 295 mOsm/kg Types of solutions according to osmolality a. Isotonic: all solutions with osmolality same as that of plasma Body cells placed in isotonic fluid: neither shrink nor swell b. Hypertonic: fluid with greater concentration of solutes than plasma Cells in hypertonic solution: water in cells moves to outside to equalize concentrations: cells will shrink c. Hypotonic: fluid with lower concentration of solutes than plasma Cells in hypotonic solution: water outside cells moves to inside of cells: cells will swell and eventually burst (hemolyze)
•Different intravenous solutions, used to correct some abnormal conditions, categorized according to osmolality: a. Hypertonic: 5%glucose, 45% NaCl solution b. Isotonic: 9% NaCl, Lactated Ringers solution c. Hypotonic: 45% NaCl B. Diffusion: solute molecules move from higher concentration to lower concentration 1. Solute, such as electrolytes, is the mover; not the water 2. Types: simple and facilitated (movement of large water-soluble molecules) C. Filtration: water and solutes move from area of higher hydrostatic pressure to lower hydrostatic pressure 1. Hydrostatic pressure is created by pumping action of heart and gravity against capillary wall
•fluids from different compartments move from one compartment to the other to maintain fluid balance.
•movement is dictated by the transport mechanism principle : A. PASSIVE B. ACTIVE TRANSPORT A. Passive Transport Process – substances transported across the membrane w/o energy input from the cell - high to low concentration 2 Types of Passive Transport 1. Diffusion – substances/solutes move from high concentration to low concentration ie exchange of O2 and CO2 b/w pulmonary capillaries and alveoli 2. Filtration – water and solutes forced through membrane by fluid or hydrostatic pressure from intravascular to interstitial area - solute containing fluid (filtrate) from higher pressure to lower pressure - an example of this process is urine formation - increased hydrostatic pressure is one mechanism producing edema B. Active Transport Process
-Cell moves substances across a membrane through ATP because:
-They may be too large -Unable to dissolve in the fat core -Move uphill against their concentration gradient Types of Active Transport 1. Active transport – requires protein carriers using ATP to energize it ie Amino acids Sodium potassium pump – 3Na out, 2K in 2. Endocytosis – moves substances into the cell 3. Exocytosis – moves substances out of the cell Osmosis
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•Movement of water from low solute to high
•10% Dextran 40 in 5% Dextrose isotonic
solute concentration in order to maintain balance between compartments. •Osmotic pressure – amount of hydrostatic pressure needed to stop the flow of water by osmosis •Oncotic pressure – osmotic pressure exerted by proteins
(252 mOsm/L)
Types of Fluid Tonicity
•This is the concentration of solutes in a solution
•A solution with high solute concentration is considered as HYPERTONIC
•A solution with low solute concentration is considered as HYPOTONIC
•A solution having the same tonicity as that of body fluid or plasma is considered ISOTONIC
•In a HYPERTONIC solution, fluid will go out from the cell, the cell will shrink.
•In a HYPOTONIC solution, fluid will enter the cell, the cell will swell.
•In an ISOTONIC solution, there will be no movement of fluid. Isotonic Fluid - no movement of fluid. Isotonic Fluids •0.9% NaCl/ Normal Saline/NSS -Na=154 -Cl=154 -308 mOsm/L - not desirable as routine maintenance solution - only solution administered with blood products Rx: hypovolemia, shock, DKA, metabolic alkalosis, hypercalcemia, mild NA deficit CI: caution in renal failure, heart failure and edema
•D5W - 5% Dextrose in water - 170 cal and free water - 252 mOsm/L Rx: hypernatremia, fluid loss and dehydration CI: early post op when ADH inc d/t stress, sole treatment in FVD (dilutes plasma), head injury (inc ICP), fluid resuscitation (hyperglycemia), caution in renal and cardiac dse (fluid overload), px with NA deficiency (peripheral circulatory collapse and anuria)
•Lactated Ringer’s Solution isotonic - Na 130 mEq/L - K 4 mEq/L -Ca 3 mEq/L - Cl 109 mEq/L - 273 mOsm/L Rx:hypovolemia, burns, fluids lost as bile/diarrhea, acute blood loss CI: ph>7.5, lactic acidosis, renal failure(cause HyperK) Hypotonic Fluid - fluid will enter the cell, the cell will swell Hypotonic Fluids
•0.45% NaCl (half strength saline) - provides Na, Cl and free water - Na 77 mEq/L - Cl 77 mEq/L - 154 mOsm/L Rx: hypertonic dehydration, Na and Cl depletion, gastric fluid loss CI : 3rd space fluid shifts and inc ICP Hypertonic Fluid - fluid will go out from the cell, the cell will shrink Hypertonic Fluids
•3% NaCl (hypertonic saline) - no calories - Na 513 mEq/L - Cl 513 mEq/L -1026 mOsm/L Rx: critical situations to treat HypoNa, assist in removing ICF excess CI: administered slowly and cautiously (IVF overload and pulmonary edema)
•5% NaCl •D10W - 10% Dextrose in water hypertonic (505 mOsm/L) •D10W - 20% Dextrose in water hypertonic (1011 mOsm/L) •D50W - 50% Dextrose in water hypertonic (1700 mOsm/L) •D5NS - 5% Dextrose & 0.9NaCl hypertonic (559 mOsm/L) •D10NS - 10% Dextrose & 0.9NaCl hypertonic (812 mOsm/L) •D5LR - 5% Dextrose in Lactated Ringers hypertonic (524 mOsm/L Colloid solutions
•Dextran 40 in NS or 5% D5W
4 - volume/plasma expander - decrease coagulation - remains for 6H in circulatory system Rx: hypovolemia in early shock, improve microcirculation (dec RBC aggregation) CI: hemorrhage, thrombocytopenia, renal disease and severe dehydration Mechanisms that Regulate Homeostasis: How the body adapts to fluid and electrolyte changes A.Thirst: primary regulator of water intake (thirst center in brain) B.Kidneys: regulator of volume and osmolality by controlling excretion of water and electrolytes C.Renin-angiotension-aldosterone mechanism: response to a drop in blood pressure; results from vasoconstriction and sodium regulation by aldosterone D.Antidiuretic hormone: hormone to regulate water excretion; responds to osmolality and blood volume E.Atrial natriuretic factor: hormone from atrial heart muscle in response to fluid excess; causes increased urine output by blocking aldosterone Organs involved in homeostasis •Kidneys •Lungs •Heart •Adrenal glands •Parathyroid glands •Pituitary glands •Other mechanisms 1. baroreceptor 2. renin-angiotensin-aldosterone system 3. ADH and thirst 4. osmoreceptor 5. release of atrial natriuretic peptide
substance and excretion of unneeded substance 3. regulation of pH of the ECF by retention of hydrogen ions 4. excretion of metabolic waste and toxic substances B. Heart and blood vessels - pumping action of the heart to maintain renal perfusion C. Lungs - maintain homeostasis through exhalation -remove approximately 300 – 400 ml of water daily -loss is greater if there is increase in respiratory depth or rate or in dry climate D. Pituitary function - hypothalamus manufactures ADH - ADH used for water retention or excretion of water by the kidney and in regulating blood volume E. Adrenal function - secretes aldosterone, has effect on fluid regulation - secretes also cortisol – has a fraction effect of aldosterone F. Parathyroid function - regulates calcium and phosphate - influences bone resorption , Ca absorption from the intestine, and Ca reabsorption from the renal tubules
•Other mechanisms: 1. baroreceptors - are small nerve receptors that detect pressure within blood vessels and transmit information to the CNS - responsible for monitoring for circulating volume and they regulate sympathetic and parasympathetic neural activity and endocrine function types: low-pressure high-pressure
•Organs involved in homeostasis A. Kidney - vital to regulation of fluid and electrolytes - filters 170 L of plasma everyday - urine output in an adult is 1-2 liters / day - releases RENIN - regulates sodium and water balance Functions include : 1. regulation of ECF volume and osmolality by selective retention and excretion of body fluids 2. regulation of electrolytes levels in the ECF by selective retention of needed
•High pressure - are nerve endings in the aortic arch and in the cardiac sinus - another is seen in the afferent arteriole of the juxtaglomerular apparatus of nephron
•Low pressure - are located in cardiac atria, particularly in the left atria 2. renin-angiotensin – aldosterone system: - renin : an enzyme that convert angiotensinogen to angiotensin I, it is released from juxtaglomerular cells of the kidney to decrease renal perfusion
5 then angiotensin I is converted to angiotensin II by angiotensin converting enzymes ,w/c is a vasoconstrictor w/c in turn increases arterial perfusion and stimulates thirst, aldosterone is released factors that influence aldosterone secretion: 1. increased release of renin 2. increased serum potassium 3. decreased Na serum 4. ACTH increase 3. ADH and THIRST - have important role in maintaining sodium concentration and oral intakes of fluids thirst: oral intake is controlled by thirst center located in the hypothalamus : serum osmolality or blood volume stimulate thirst center ADH - controls water excretion - determines concentration of urine 4. osmoreceptors - located in the surface of hypothalamus - sense changes in Na concentration osmotic pressure (neurons become dehydrated) releases impulses to posterior pituitary to release ADH increases permeability of membrane to H2O (kidney, causing reabsorption of water and urine output)
decreased
5. Release of atrial natriuretic peptide released by cardiac cells in the atria of the heart in response to increased atrial pressure - action of this is direct opposite of RAAS and decreases blood pressure and volume - ANP level is 20 to 77 pg /ml (ng/ml) Regulation of Body Fluid
1. The Kidney
•Regulates primarily fluid output by urine formation 1.5L
•Releases RENIN •Regulates sodium and water balance 2. Endocrine regulation
•thirst mechanism – thirst center in hypothalamus
•ADH increases water reabsorption on collecting duct
•Aldosterone increases Sodium and water retention retention in the distal nephron
•ANP Promotes Sodium excretion and inhibits thirst mechanism 3. Gastro-intestinal regulation - GIT digests food and absorbs water - Only about 200 ml of water is excreted in the fecal material per day 4. Heart and Blood Vessel Functions - pumping action of heart circulates blood through kidneys 5. Lungs – insensible water loss through respiration Other Mechanisms 1. Baroreceptors – carotid sinus and aortic arch - causes vasoconstriction and increased blood pressure Dec arterial pressure SNS inc cardiac rate, contraction, contractility, circulating blood volume, constriction of renal arterioles and increased aldosterone 2. Osmoreceptors – surface of hypothalamus senses changes in Na concentration Inc osmotic pressure neurons dehydrated release ADH KIDNEY •Nephron: glomerulus and tubule •Filtration •Retention/ Reabsorption •Excretion •170-180 L/day •Filtrate= urine (1-2 L urine/ day) •Fluid excess excretes dilute urine (rids body of excess fluid while conserving electrolytes)
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ADH (Antidiuretic hormone)
•Vasopressin •Water-retainer •Hypothalamus produces ADH •Posterior pituitary gland stores and releases ADH
•Restores
blood volume by reducing diuresis and increasing water retention ADH Low blood volume/ Pituitary gland Increased serum osmolality secretes ADH into the bloodstream ADH causes the Water retention Kidneys to retain water increases blood volume/ decreases serum osmolality ADH Regulation
•ADH - produced by the Hypothalamus - stored and secreted by the posterior pituitary gland
•less water in plasma,
ADH secreted to conserve water by reducing urine output
•fluid overload in plasma,
ADH secretion stops to excrete fluid in the kidneys by increasing urine output ADH Disorder
•Abnormally high ADH concentration SIADH reduced urine output (oliguria) water retention (fluid overload)
•Abnormally low ADH – Diabetes Insipidus increased urine output (polyuria) water loss (fluid deficit) ADH Disorder •SIADH –Abnormally high ADH concentration –urine output is reduced (oliguria) –water retention (fluid overload) –Urine SG is high (normal: 1.005 – 1.030) –Hct is low (43-48%)
•DI –Abnormally low ADH –urine output is increased (polyuria) –water loss (fluid deficit)
–Urine SG is low –Hct is high RAAS (Renin-Angiotensin-Aldosterone System) •To help maintain a balance of sodium and water, a healthy blood volume and blood pressure, the juxtaglomerular cells near each glomerulus secrete RENIN •Leads to production of Angiotensin II, a powerful vasoconstrictor •Angiotensin II causes peripheral vasoconstriction, stimulating production of Aldosterone •Both increase blood pressure. Aldosterone Production Decreased JG cells Renin travels blood flow to the secrete to the glomerulus Renin liver Renin converts Angiotension 1 Angiotensin 1 Angiotensin in travels to the in the lungs is the liver to lungs converted to Angiotensin 1 Angiotensin II Angiotensin II travels to the Adrenal glands
Angiotensin II stimulates the adrenal glands to produce
Aldosterone Aldosterone Angiotensin II
Aldosterone Sodium and
stimulates the causes kidneys water retention adrenal glands to to retain sodium leads to increased produce Aldosterone and water fluid volume and
sodium level Aldosterone Disorders
•Addison’s Disease –Abnormally low aldosterone –Serum Na is low, serum potassium is high
7 decrease ADH increase GFR w/c increases
–FVD
•Cushing’s Disease –Abnormally high aldosterone –Serum Na is high, serum potassium is low –FVE
Suppression of serum renin
ANP (Atrial Natriuretic Peptide)
•Cardiac hormone •Stored in the cells of the atria •Released when atrial pressure increases •Counteracts the effects of the RAAS by decreasing blood pressure and reducing intravascular blood volume
•When blood volume and BP rise and stretch the atria, ANP shuts off RAAS ANP •Suppresses serum renin levels •Decreases aldosterone release from the adrenal glands •Increases glomerular filtration, which increases urine excretion of sodium and water •Decreases ADH release from the posterior pituitary gland •Reduces vascular resistance by causing vasodilation Examples of causes of atrial stretching (which result to increased release of ANP)
•Orthostatic changes •Atrial tachycardia •High sodium intake •Sodium chloride infusions •Use of drugs that cause vasoconstriction •Physiology/pathophysiology
increased blood volume increased blood pressure increased stretch of atria increased ANP release vascular resistance
urinary excretion of Na and Decrease blood pressure water
decrease vascular volume decrease BP, decrease preload and afterload Thirst mechanism •Regulated by the hypothalamus •Stimulated by an increase in ECF and drying of mucous membrane •Causes a person to drink fluids, which is absorbed by the intestines, moved to the bloodstream and distributed between the compartments •Leads to increased amount of fluid in the body and a decrease in concentration of solutes Decreased Blood Volume THIRST mechanism
•ADH secretion is increased •ANP secretion is decreased •RENIN secretion is increased •BARORECEPTOR vasoconstricton •ALDOSTERONE secretion is increased Increased Blood Volume
•NO THIRST mechanism •ADH secretion is decreased •ANP secretion is increased •RENIN secretion is increased •BARORECEPTOR vasodilation •ALDOSTERONE decreased Fluid status can be assessed through:
•Mucus membrane •Skin integrity •Body weight •Jugular vein •BP, PAWP 6-12 mm Hg •CVP (most accurate) 0-7 mm Hg or 5-10 cm of H2O •I&O •Pulse •Temperature
8 •Lung sound and heart sound •Urine output •Urine SG 1.005-1.030 •Hematocrit 48% •Plasma osmolality •LOC
•byproduct of muscle metabolism &
Evaluation of fluid status Osmolality – concentration of fluid that affects movement of water between fluid compartments by osmosis - measures the solute concentration per kg in blood and urine - measure of solution’s ability to create osmotic pressure and affect the movement of sodium
•better indicator of • .7 to 1.5 mg/dl
excreted by kidneys regardless of fluid intake, diet, etc.
•measures kidney function; 50%
- reported as mOsm/kg - normal value= 280-300 mOsm/kg Osmolarity – concentration of solutions - measures the solute concentration per L in blood and urine - mOsm/L urine specific gravity - measures the kidneys ability to excrete or conserve water urine specific gravity: 1.010 - 1.025 Blood urea nitrogen - made up of urea, end product of metabolism of protein 10-20mg/dl (3.5-7mmol/l) BUN: not most reliable indicator of renal disease BUN:creatinine ratio better indicator Normal 10:1. increased BUN due to: 1. renal function 2. GI bleeding 3. dehydration 4. increased protein intake 5. fever and sepsis decreased BUN due to : 1. end-stage liver disease 2. low protein
renal function lost BEFORE ↑ in serum creatinine level renal function
Hematocrit - indication of hydration status measures the volume percentage of red blood cells in whole blood and normally ranges from 44% to 52% for male 39% - 47% in females hematocrit due to:
1. dehydration 2. polycythemia
hematocrit due to:
1. overhydration 2. anemia
•Urine sodium values: change with sodium intake and status of fluid volume - normal level ranges from 50 220mEq/24h - used to assess volume status and in the diagnosis of hyponatremia and acute renal failure Fluid volume disturbances
•I and O must be equal •2.5 L per day •Fluid volume deficit (hypovolemia) •Fluid volume excess (hypervolemia) I&O Imbalance Fluid Volume Deficit •↑output, normal intake •Normal output, ↓ intake •No intake
intake 3. starvation 4.condition that expands fluid volume ex. pregnancy Creatinine
Fluid Volume Excess •↑ intake, normal output •Normal intake, ↓ output •No output
9 1. Fluid volume deficit - occurs when loss of ECF volume exceeds the intake of fluid causes: 1. abnormal fluid losses vomiting, diarrhea, GI suctioning and sweating Diabetes Insipidus Adrenal insufficiency Osmotic diuresis Hemorrhage 3rd space fluid shift 2. decreased intake
signs and symptoms : 1. acute weight loss 2. decreased skin turgor 3. oliguria 4. concentrated urine 5. postural hypotension, weak and rapid heart rate 6. flattened neck veins, decreased CVP, cool clammy skin 7. Thirst, anorexia 8. Muscle weakness and cramps Assessment of FVD
•ICF cellular dehydration
•ITF skin
poor skin turgor
•IVF artery vein
↓BP, pulse (rapid thready) ↓CVP
assessment : 1. elevated BUN 2. elevated Hct. 3. serum electrolyte changes may also exist 1. hypokalemia- GI and renal losses 2. hyperkalemiaadrenal insufficiency 3. hyponatremiaincreased thirst and ADH release 4. hypernatremiaincreased insensible losses and diabetes insipidus Medical Management
•Oral intake when mild •IV route, acute or severe
•Isotonic fluids ie LR lactated ringers or .9% NaCl for hypotensive patients to expand plasma volume Nursing Management
•measure I and O accurately •monitoring of body weight - loss of .5 kg means a loss of 500ml
•monitoring of V/S •skin turgor assessment •Assess CVP, LOC, breath sounds and skin color •Monitor urinary concentration •Monitor mental function
2. fluid volume excess (hypervolemia) - refers to an isotonic expansion of the ECF caused by the abnormal retention of water and Na in approx. same proportion - usually 2nd to increase in total body Na content Pathophysiology: 1. related to simple fluid overload 2. diminished function of the homeostatic mechanism responsible for regulating fluid balance Causes of FVE
•Heart failure •renal failure •cirrhosis of the liver •consumption of excessive amount of salt •Excessive administration of Na containing fluids in a patient w/ impaired regulatory mechanism
•SIADH Clinical Manifestations •Distended neck veins •Tachycardia •Inc weight •Increased urine output •Shortness of breath and wheezing/ crackles •Inc CVP •Edema •increased BP •increased pulse pressure
10 Assessment of FVE
•ICF cellular edema - ↓LOC pulmonary edema - crackles (bibasilar), wheezing, shortness of breath, Inc RR
•Assess breath sounds •Monitor degree of edema ie ambulatory – feet and ankles bedridden – sacral area •Promote rest – favors diuresis/inc venous return •Administer appropriate medication
•ITF skin - bipedal pitting edema, periorbital edema and ANASARCA
•IVF artery - ↑BP, pulse (rapid bounding) vein - ↑CVP Edema
•common manifestation of FVE •d/t inc capillary fluid pressure, decreased capillary oncotic pressure, increased interstitial oncotic pressure
•Localized or generalized •Etiology: obstruction to lymph flow, plasma albumin level < 1.5-2 g/dl, burns and infection, Na retention in ECF, drugs
•Labs: Dec Hct, respiratory alkalosis and hypoxemia, dec serum Na and osmolality, inc BUN Crea, Dec Urine SG, dec urine Na level
•Mgmt: diuretics, fluid restriction, elevation of extremities, elastic compression stockings, paracentesis, dialysis Laboratory (FVE)
•Dec BUN •Dec Hct •CRF – serum osmolality and Na level dec •chest x-ray may reveal pulmonary congestion Medical Management •Discontinue administration of Na solution •Diuretics ie Thiazide – block Na reabsorption in distal tubule Loop diuretics – block Na reabsorption in ascending loop of Henle •Restrict fluid and salt intake •Dialysis Nursing Management •Measure intake and output •Weigh patient daily 2 lb wt gain = 1 L fluid
Electrolytes
•elements or compounds when dissolved in water will dissociate into ions and are able to conduct an electric current. FUNCTIONS: 1. Regulate fluid balance and osmolality 2. Transmission of nerve impulse 3. Stimulation of muscle activity
•ANIONS - negatively charged ions: Bicarbonate, chloride, PO4-, CHON
•CATIONS - positively charged ions: Sodium, Potassium, magnesium, calcium Cations Sodium , Potassium , Calcium , Magnesium , hydrogen ions Anions Chloride, bicarbonate , phosphate, sulfate, proteinate ions
•Sodium - positively charged ions , major cation in the ECF -important in regulating the volume of body fluids -retention of Na- associated with fluid retention -loss of Na- decreased volume of body fluids
•Potassium - major cation in the ICF •Chloride - major anion in the ECF •Phosphate - major anion in the ICF Regulation of Electrolyte Balance 1. Renal regulation •Occurs by the process of glomerular filtration, tubular reabsorption and tubular secretion •Urine formation
11 –If there is little water in the body, it is conserved –If there is water excess, it will be eliminated 2. Endocrinal regulation •Aldosterone promotes Sodium retention and Potassium excretion •ANP promotes Sodium excretion •Parathormone increased bone resorption of Ca, inc Ca reabsorption from renal tubule or GI tract •Calcitoninoppose PTH •Insulin and Epinephrine – promotes uptake of Potassium by cells The Cations
•SODIUM •POTASSIUM •CALCIUM •MAGNESIUM
Dx: inc serum sodium and Cl level, inc serum osmolality, inc urine sp.gravity, inc urine osmolality Mgmt: sodium restriction, water restriction, diuretics, isotonic non saline soln. (D5W) or hypotonic soln, Desmopressin Acetate for Diabetes Insipidus Nsg considerations History – diet, medication Monitor VS, LOC, I and O, weight, lung sounds Monitor Na levels Oral care initiate gastric feedings slowly Seizure precaution b. HYPONATREMIA
•Na < 135 mEq/L •Etiology: diuretics, excessive sweating,
SODIUM (Na)
vomiting, diarrhea, SIADH, aldosterone deficiency, cardiac, renal, liver disease
•MOST ABUNDANT cation in the ECF •135-145 mEq/L •Aldosterone increases sodium
•Dx: dec serum and urine sodium and
reabsorption •ANP increases sodium excretion •Cl accompanies Na
•s/sx: headache, apprehension, restlessness,
FUNCTIONS: 1. assists in nerve transmission and muscle contraction 2. Major determinant of ECF osmolality 3. Primary regulator of ECF volume a. HYPERNATREMIA
•Na > 145 mEq/L •Assoc w/ water loss or sodium gain •Etiology: inadequate water intake, excessive salt ingestion /hypertonic feedings w/o water supplements, near drowning in sea water, diuretics, Diabetes mellitus/ Diabetes Insipidus
S/SX: polyuria, anorexia, nausea, vomiting, thirst, dry and swollen tongue, fever, dry and flushed skin, restlessness, agitation, seizures, coma, muscle weakness, crackles, dyspnea, cardiac manifestations dependent on type of hypernatremia
osmolality, dec Cl
altered LOC, seizures(<115meq/l),coma, poor skin turgor, dry mucosa, orthostatic hypotension, crackles, nausea, vomiting, abdominal cramping Mgmt: sodium replacement, water restriction, isotonic soln for moderate hyponatremia, hypertonic saline soln for neurologic manifestations, diuretic for SIADH Nsg. Consideration Monitor I and O, LOC, VS, serum Na Seizure precaution diet Potassium (K) •MOST ABUNDANT cation in the ICF •3.5-5.5 mEq/L •Major electrolyte maintaining ICF balance •maintains ICF Osmolality •Aldosterone promotes renal excretion of K+ •Mg accompanies K FUNCTIONS:
12 1. nerve conduction and muscle contraction 2. metabolism of carbohydrates, fats and proteins 3. Fosters acid-base balance a. HYPERKALEMIA
•K+ > 5.0 mEq/L •Etiology: IVF with K+, acidosis, hyperalimentation and excess K+ replacement, decreased renal excretion, diuretics, Cancer
•s/sx: nerve and muscle irritability, tachycardia, colic, diarrhea, ECG changes, ventricular dysrythmia and cardiac arrest, skeletal muscle weakness, paralysis
•Dx: inc serum K level ECG: peaked T waves and wide QRS ABGs – metabolic acidosis
ECG - flattened , depressed T waves, presence of “U” waves ABGs - metabolic alkalosis Medical Mgmt: diet ( fruits, fruit juices, vegetables, fish, whole grains, nuts, milk, meats) oral or IV replacement Nsg mgmt: monitor cardiac function, pulses, renal function monitor serum potassium concentration IV K diluted in saline monitor IV sites for phlebitis Normal ECG Hypokalemia Hyperkalemia
Mgmt: K restriction (coffee, cocoa, tea, dried fruits, beans, whole grain breads, milk, eggs) diuretics Polystyrene Sulfonate (Kayexalate) IV insulin Beta 2 agonist IV Calcium gluconate – WOF Hypotension IV NaHCo3 – alkalinize plasma Dialysis Nsg consideration: Monitor VS, urine output, lung sounds, Crea, BUN monitor K levels and ECG observe for muscle weakness and dysrythmia, paresthesia and GI symptoms
Regulation: •GIT absorbs Ca+ in the intestine with the help of Vitamin D •Kidney Ca+ is filtered in the glomerulus and reabsorbed in the tubules •PTH increases Ca+ by bone resorption, inc intestinal and renal Ca+ reabsorption and activation of Vitamin D •Calcitonin reduces bone resorption, increase Ca and Phosphorus deposition in bones and secretion in urine a. HYPERCALCEMIA
•Serum calcium > 10.5 mg/dL •Etiology: Overuse of calcium supplements
•K+ < 3.5 mEq/L
and antacids, excessive Vitamin A and D, malignancy, hyperparathyroidism, prolonged immobilization, thiazide diuretic
•Etiology: use of diuretic, corticosteroids
•s/sx: anorexia, nausea, vomiting, polyuria,
and penicillin, vomiting and diarrhea, ileostomy, villous adenoma, alkalosis, hyperinsulinism, hyperaldosteronism
•Dx: inc serum Ca
b. HYPOKALEMIA
•s/sx: anorexia, nausea, vomiting, decreased bowel motility, fatigue, muscle weakness, leg cramps, paresthesias, shallow respiration, shortness of breath, dysrhythmias and increased sensitivity to digitalis, hypotension, weak pulse, dilute urine, glucose intolerance Dx: dec serum K level
muscle weakness, fatigue, lethargy ECG: Shortened QT interval, ST segments inc PTH levels xrays - osteoporosis
•Mgmt: 0.9% NaCl IV Phosphate Diuretics – Furosemide IM Calcitonin corticosteroids
13 dietary restriction (cheese, ice cream, milk, yogurt, oatmeal, tofu) Nsg Mgmt: Assess VS, apical pulses and ECG, bowel sounds, renal function, hydration status safety precautions in unconscious patients inc mobility inc fluid intake monitor cardiac rate and rhythm b. HYPOCALCEMIA •Calcium < 8.5 mg/dL
•Etiology: removal of parathyroid gland during thyroid surgery, Vit. D and Mg deficiency, Furosemide, infusion of citrated blood, inflammation of pancreas, renal failure, thyroid CA, low albumin, alkalosis, alcohol abuse, osteoporosis (total body Ca deficit)
•
s/sx: Tetany, (+) Chovstek’s (+) Trousseaus’s, seizures, depression, impaired memory, confusion, delirium, hallucinations, hypotension, dysrythmia
DKA, adrenocortical insufficiency
•s/sx: hypotension, nausea, vomiting, flushing, lethargy, difficulty speaking, drowsiness, dec LOC, coma, muscle weakness, paralysis, depressed tendon reflexes, oliguria, ↓RR
•Mgmt: discontinue Mg supplements Loop diuretics IV Ca gluconate Hemodialysis Nsg mgmt: monitor VS observe DTR’s and changes in LOC seizure precautions b. HYPOMAGNESEMIA •Mg < 1.5 mEq/l
•Etiology: alcohol w/drawal, tube feedings, diarrhea, fistula, GIT suctioning, drugs ie antacid, aminoglycosides, insulin therapy, sepsis, burns, hypothermia
•Dx:
•s/sx: hyperexcitability w/ muscle weakness,
dec Ca level ECG: prolonged QT interval
tremors, tetany, seizures, stridor, Chvostek and Trousseau’s signs, ECG changes, mood changes
•Mgmt: Calcium salts Vit D
•Dx: serum Mg level
diet (milk, cheese, yogurt, green leafy vegetables)
ECG – prolonged PR and QT interval, ST depression, Widened QRS, flat T waves low albumin level
•Nsg mgmt
•Mgmt:
monitor cardiac status, bleeding monitor IV sites for phlebitis seizure precautions reduce smoking Magnesium Mg
•Second to K+ in the ICF •Normal range is 1.3-2.1 mEq/L FUNCTIONS 1. intracellular production and utilization of ATP 2. protein and DNA synthesis 3. neuromuscular irritability 4, produce vasodilation of peripheral arteries a. HYPERMAGNESEMIA
•M > 2.1 mEq/L •Etiology: use of Mg antacids, K sparing diuretics, Renal failure, Mg medications,
diet (green leafy vegetables, nuts, legumes, whole grains, seafood, peanut butter, chocolate) IV Mg Sulfate via infusion pump
•Nsg Mgmt: seizure precautions Test ability to swallow, DTR’s Monitor I and O, VS during Mg administration The Anions
•CHLORIDE •PHOSPHATES •BICARBONATES Chloride (Cl) •The MAJOR Anion in the ECF •Normal range is 95-108 mEq/L
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•Inc Na reabsorption causes increased Cl reabsorption FUNCTIONS 1. major component of gastric juice aside from H+ 2. together with Na+, regulates plasma osmolality 3. participates in the chloride shift – inverse relationship with Bicarbonate 4. acts as chemical buffer a. HYPERCHLOREMIA
•Serum Cl > 108 mEq/L •Etiology: sodium excess, loss of bicarbonate ions
•s/sx: tachypnea, weakness, lethargy, deep rapid respirations, diminished cognitive ability and hypertension, dysrhytmia, coma
•Dx: inc serum Cl dec serum bicarbonate Mgmt: Lactated Ringers soln IV Na Bicarbonate Diuretics Nsg mgmt: monitor VS, ABGs, I and O, neurologic, cardiac and respiratory changes b. HYPOCHLOREMIA •Cl < 96 mEq/l
•Etiology: Cl deficient formula, salt restricted diets, severe vomiting and diarrhea
•s/sx: hyperexcitability of muscles, tetany, hyperactive DTR’s, weakness, twitching, muscle cramps, dysrhytmias, seizures, coma
•Dx: dec serum Cl level ABG’s – metabolic alkalosis Mgmt: Normal saline/half strength saline diet ( tomato juice, salty broth, canned vegetables, processed meats and fruits avoid free/bottled water) Nsg mgmt: monitor I and O, ABG’s, VS, LOC, muscle strength and movement Phosphates (PO4) •The MAJOR Anion in the ICF •Normal range is 2.5-4.5 mg/L •Reciprocal relationship w/ Ca
•PTH inc bone resorption, inc PO4 absorption from GIT, inhibit PO4 excretion from kidney •Calcitonin increases renal excretion of PO4 FUNCTIONS 1. component of bones 2. needed to generate ATP 3. components of DNA and RNA a. HYPERPHOSPHATEMIA
•Serum PO4 > 4.5 mg/dL •Etiology: excess vit D, renal failure, tissue trauma, chemotherapy, PO4 containing medications, hypoparathyroidism
•s/sx: tetany, tachycardia, palpitations, anorexia, vomiting, muscle weakness, hyperreflexia, tachycardia, soft tissue calcification
•Dx: inc serum phosphorus level dec Ca level xray – skeletal changes Mgmt: diet – limit milk, ice cream, cheese, meat, fish, carbonated beverages, nuts, dried food, sardines Dialysis Nsg mgmt: dietary restrictions monitor signs of impending hypocalcemia and changes in urine output b. HYPOPHOSPHATEMIA •Serum PO4 < 2.5 mg/dl
•Etiology: administration of calories in severe CHON-Calorie malnutrition (iatrogenic), chronic alcoholism, prolonged hyperventilation, poor dietary intake, DKA, thermal burns, respiratory alkalosis, antacids w/c bind with PO4, Vit D deficiency
•s/sx: irritability, fatigue, apprehension, weakness, hyperglycemia, numbness, paresthesias, confusion, seizure, coma
•Dx: dec serum PO4 level Mgmt: oral or IV Phosphorus correction diet (milk, organ meat, nuts, fish, poultry, whole grains)
15 Nsg mgmt: introduce TPN solution gradually prevent infection
•Fluids •Electrolytes •Acid-Base •Burns •Shock •GUT •MASTERY
D1 D2 D3 D3 D4 D5 D6
- kidney excrete H and reabsorbs/generates Bicarbonate 2. RESPIRATORY/METABOLIC ALKALOSIS - kidney retains H ion and excrete Bicarbonate Lung -Control CO2 and Carbonic acid content of ECF 1. METABOLIC ACIDOSIS - increased RR to eliminate CO2 2. METABOLIC ALKALOSIS - decreased RR to retain CO2
Acid Base Balance
•Acid - substance that can donate or release hydrogen ions ie Carbonic acid, Hydrochloric acid ** Carbon dioxide – combines with water to form carbonic acid
•Base
•pH -
measures degree of acidity and alkalinity - indicator of H ion concentration - Normal ph 7.35-7.45
•ACIDOSIS - decreased pH; < 7.35 - increased Hydrogen
- substance that can accept hydrogen ions Ie Bicarbonate
•ALKALOSIS •BUFFER- substance that can accept or donate hydrogen - prevent excessive changes in pH TYPES OF BUFFER 1. Bicarbonate (HCO3): carbonic acid buffer (H2CO3) 2. Phosphate buffer 3. Hemoglobin buffer Dynamics of Acid Base Balance •Acids and bases are constantly produced in the body •They must be constantly regulated •CO2 and HCO3 are crucial in the balance •A HCO3:H2CO3 ratio of 20:1 should be maintained •Respiratory and renal system are active in regulation Kidney - Regulate bicarbonate level in ECF 1. RESPIRATORY/METABOLIC ACIDOSIS
- increased pH-; > 7.45 - decreased Hydrogen ACUTE AND CHRONIC METABOLIC ACIDOSIS
-Low pH -Increased H ion concentration -Low plasma Bicarbonate Etiology: diarrhea, fistulas, diuretics, renal insufficiency, TPN w/o Bicarbonate, ketoacidosis, lactic acidosis S/sx: headache, confusion, drowsiness, inc RR, dec BP, cold clammy skin, dysrrythmia, shock
•Dx: ABG – low Bicarbonate, low pH, Hyperkalemia, ECG changes
•Rx: Bicarbonate for pH < 7.1 and Bicarbonate level < 10 monitor serum K dialysis ACUTE AND CHRONIC METABOLIC ALKALOSIS •High pH •Decreased H ion concentration
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•High plasma Bicarbonate
ARTERIAL BLOOD GAS ANALYSIS
Etiology: vomiting, diuretic, hyperaldosteronism, hypokalemia, excesive alkali ingestion
Evaluating ABG’s
s/sx: tingling of toes, dizziness, dec RR, inc PR, ventricular disturbances
•Dx:ABG – pH > 7.45, serum Bicarbonate >
Note the pH pH = 7.35 – 7.45 (normal) pH = < 7.35 (acidosis) pH = > 7.45 (alkalosis) compensated – normal pH uncompensated – abnormal pH
26 mEq/L, inc PaCO2
•Rx: restore normal fluid balance correct hypokalemia Carbonic anhydrase inhibitors ACUTE AND CHRONIC RESPIRATORY ACIDOSIS •Ph < 7.35 PaCO2 > 42 mmHg
2. Determine primary cause of disturbance 2.1 pH > 7.45 a. PaCo2 < 40 mmHg – respiratory alkalosis b. HCO3 > 26 mEq/L – metabolic alkalosis 2.2 pH < 7.35 a. PaCo2 > 40 mmHg – respiratory acidosis b. HCO3 < 26 mEq/L – metabolic acidosis
Etiology: pulmonary edema, aspiration, atelectasis, pneumothorax, overdose of seatives, sleep apnea syndrome, pneeumonia
3. Determine compensation by looking at the value other than the primary disturbance
s/sx: sudden hypercapnia produces inc PR, RR, inc BP, mental cloudinesss, feeling of fullness in head, papiledema and dilated conjunctival blood vessels
4. Mixed acid-base disorders
•Dx: ABG – pH < 7.35 PaCO2 - > 42 mmHg
•Rx: improve ventilation pulmonary hygiene mechanical ventilation
ACUTE AND CHRONIC RESPIRATORY ALKALOSIS •pH > 7.45 •PaCO2 < 38 mmHg Etiology: extreme anxiety, hypoxemia s/sx: lightheadednes, inability to concentrate, numbness, tingling, loss of consciousness
•Dx: ABG – pH > 7.45 PaCO2 < 35 dec K dec Ca Rx: breathe slowly sedative
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