fluid volume deficit body's fluid intake isnt sufficient to meet body's fluid needs fluid volume deficit causes (GID VIC) GI suctioningIleostomy or colostomy drainageDraining wounds, burns, or fistulas Vomiting or diarrheaIncreased urine output from use of diureticsContinuous GI irrigation fluid volume deficit s/s(THIRDD FPIC) ThirstHR increases, thready pulse,and postural hypotensionIncreased specific gravity of urineRapid weight lossDizziness or weaknessDecrease in urine, dark, cloudy, concentrated Flat neck and hand veinPoor skin turgor and dry mucous membranesIncreased Prepared by: Edwin DR Abu Exclusive for BSN IV D&E use ONLY.
GI suctioningIleostomy or colostomy drainageDraining wounds, burns, or fistulas
Vomiting or diarrheaIncreased urine output from use of diureticsContinuous GI irrigation
fluid volume deficit s/s(THIRDD FPIC)
ThirstHR increases, thready pulse,and postural hypotensionIncreased specific gravity of urineRapid weight lossDizziness or weaknessDecrease in urine, dark, cloudy,
concentrated
Flat neck and hand veinPoor skin turgor and dry mucous membranesIncreased hematocrit levelConfusionIncreased
Give with food/juice (causes GI irritation)IV site (watch for phlebitis, infiltration)Monitor VSMonitor I&OMonitor neuromuscular activityMonitor cardiac changesMonitor
electrolyte level
hyperkalemia intervention(M^5AP)
Monitor VSMonitor for cardiac changesMonitor I&OMonitor Lab valuesMonitor for calcium and magnesium loss when
using KayexalateAdm. sodium polystyrene sulfonate (Kayexalate)Prepare for peritoneal dialysis, hemodialysis (as
prescribed)
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sodium levels 135 to 145 mEg/L
hyponatremia causes(IN BIG DIPER)
Irrigation of GI tubes with plain waterNausea and vomiting
Long term immobilization and bone demineralizationInadequate Vit. D consumptionEnd stage
renal disease
Decreased secretion of parathyroid hormoneInhibited absorption of calcium from the intestinal tractExcessive GI
losses from diarrhea or wound draining
Inadequate intake of calciumExcessive adm. of blood
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hypocalcemia s/s(HHC TTT PPP )
HypotensionHyperactive bowelsCrampsDiarrhea
TachycardiaTwitchingTetany
ParesthesiasPositive Chovestek's or Trousseau's signProlongation of QT interval
hypocalcemia interventions(TIM AAMP KIM)
Teach client proper use of antacids or laxativeInstruct client taking calcium excreting meds to check CA levels
periodicallyMonitor calcium levels closely
Adm. Vit. D (AP) to aid in the digestion of calcium from the intestinal tractAdm. CA 1-2 hours after meal to max.
intestinal absorptionMonitor VSProvide quiet environment, avoid over stimulation
Keep 10% calcium gluconate for acute calcium deficitInitiate seizure precautionsMonitor for Chvostek's (contraction of
facial muscles in response to a light tap over the facial nerve in front of the ear) Trousseau's )carpal spasm induced by
inflating a BP cuff above systolic pressure for a few minutes.)
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hypercalcemia causes(RH AEIU)
Renal failureHyperparathyroidism
Adrenal insufficiency Excessive intake of Vit. DIncreased bone resorption of destruction from conditions (tumors, fractures, osteoporosis, & immobility)Use of thiazide,
lithium, glucocorticoids
hypercalcemia s/s(MIND ABBCC)
Muscle weakness (hypotonicity)Increased HR & BPNausea and vomitingDiminished deep tendon reflexes
Abdominal distentionBounding pulseBradycardia(late stage)ConstipationConfusion, lethargy, and coma
hypercalcemia reading T wave- widenedQT interval shortened
Monitor neuromuscular irritabilityMonitor for hyperreflexia, tetany,a nd seizuresMonitor for Trosseau's and Chvostek's signMonitor for signs of hypocalcemiaAdm. calcium(AP)if hypocalcemia existsTake with meals or immediately after
meals.
Prepared by: Edwin DR Abu
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phosphorus food sourcesNutsOrgan meatsWhole grain breads and cereals
FishPork, beef, chicken
daily body fluid excretion or lossskin(diffusion) 400mlskin(perspiration) 100mllungs
350mlfeces 150mlkidneys 1500ml
Isotonic solutions5% dextrose in water5% dextrose in 0.225% salineLactated
Ringers Solution0.9% saline
hypotonic 0.45 saline
hypertonic5% dextrose in Lactated Ringer solution5% dextrose in 0.45% saline5% dextrose in 0.9% saline10% dextrose in
water
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Third spacingThe accumulation of trapped extracellular fluid in a body
space due to disease or injury
Acidosis or AlkalosisSleuthing: Using Blood Values to determine the Cause of Acidosis or Alkalosis
Note the pH. This tells you whether the person is in acidosis (pH < 7.35) or alkalosis (pH > 7.45); but it does not tell you the cause.
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Next, check the PCO2 to see if this is the cause of the acid-base imbalance. Because the respiratory system is a fast-acting system, an excessively high or low PCO2 may indicate either that the condition is respiratory system—caused or that the respiratory system is compensating. For example, if the pH indicates acidosis and:The PCO2 is over 45 mm Hg, the respiratory system is the cause of the problem and the condition is a respiratory acidosis.The PCO2 is below normal limits (below 35 mmHg), the respiratory system is not the cause but is compensating.The PCO2 is within normal limits; the condition is neither caused nor compensated by the respiratory system.Check the bicarbonate level. If step 2 proves that the respiratory system is not responsible for the imbalance, then the condition is metabolic and should be reflected in increased or decreased bicarbonate levels. Metabolic acidosis is indicated by HCO3- values below 22 mEq/L, and metabolic alkalosis by values over 26 mEq/L. Notice that whereas PCO2 vary inversely with blood pH (PCO2 rises as blood pH falls), HCO3- levels vary directly with blood pH (increased HCO3- results in increased pH). Beyond this bare-bones approach there is something else to consider when you are assessing acid-base problems. If an imbalance is fully compensated, the pH may be normal even when the pH is normal, carefully scrutinize the PCO2 or HCO3- values for clues to what imbalance may be occurring.
Causes and Consequences of Acid-Base imbalances
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Metabolic acidosis:
Uncompensated (uncorrected) HCO3- < 22 mEq/L; pH < 7.4Severe diarrhea: Bicarbonate-rich intestinal (and pancreatic) secretions rushed through digestive tract before their solutes can be reabsorbed; bicarbonate ions are replaced by renal mechanisms that generate new bicarbonate ions.Renal disease: failure of the kidneys to rid body of acids formed by normal metabolic processes.Untreated diabetes mellitus: lack of insulin or inability of tissue cells to respond to insulin, resulting in inability to use glucose; fats are used as primary energy fuel, and ketoacidosis occurs.Starvation: Lack of dietary nutrients for cellular fuels, body proteins and fat reserves are used for energy—both yield acidic metabolites as they are broken down for energy.High ECF potassium concentrations: Potassium ions compete with H+ for secretion in renal tubules; when ECF levels of K+ are high, H+ secretion is inhibited.Metabolic alkalosis:
Uncompensated (HCO3- >26 mEq/L; pH > 7.4)Vomiting or gastric suctioning: loss of stomach HCl requires that H+ be withdrawn from blood to replace stomach acids; thus H+ decreases and HCO3- proportionally.Selected diuretics: cause K+ depletion and H2O loss. Low K+ directly stimulates the tubule cells to secrete H+. Reduced blood volume elicits the renin-angiotensin mechanism, which stimulates Na+ reabsorption and H+ secretion.Ingestion of excessive sodium bicarbonate (antacid): bicarbonate moves easily into ECF, where it enhances natural alkaline reserve.Constipation: prolonged retention of feces, resulting in increased amounts of HCO3- being reabsorbed.
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Excessive aldosterone: (adrenal tumors) promotes excessive reabsorption of Na+, which pulls increased amount of H+ into urine. Hypovolemia promotes the same relative effect because aldosterone secretion is increased to enhance Na+ (and H2O) reabsorption.
Respiratory acidosis:
Uncompensated (PCO2 >45 mm Hg; pH <7.4)Impaired gas exchange or lung ventilation (chronic bronchitis, cystic fibrosis, emphysema): Increased airway resistance and decreased expiratory air flow, leading to retention of carbon dioxide.Rapid, shallow breathing: Tidal volume markedly reduced.Narcotic or barbiturate overdose or injury to the brain stem: depression of respiratory centers, resulting in hypoventilation and respiratory arrest.
Respiratory alkalosis:
Uncompensated (PCO2 < 35 mm Hg; pH > 7.4)Direct cause is always hyperventilation: hyperventilation is pain/anxiety, asthma, pneumonia, and at high altitude represents effort to raise PO2 at the expense of excessive carbon dioxide excretion.Brain injury or tumor: abnormality of respiratory controls.
