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DTC 330

EN, PN, and Acid Base

Nausea/Vomiting Treatment reducing/discontinuing narcotic medications Switch to a lowfat formula Administer feeding solution at room temperature Reduce rate of infusion by 20-25 ml/hr Administer prokinetic agent Check gastric residuals Consider antiemetics
Fluid and Electrolyte Disturbances May result from long term nutrition deficits, acute stress, medications, medical conditions, improper nutrient prescription Electrolytes lost via stool, urine, ostomy or fistula drainage Dehydration most common complication especially with high protein
Refeeding Syndrome At risk: when refeeding those with marginal body nutrient stores, stressed, depleted patients, those who have been unfed for 7-10 days, persons with anorexia nervosa, chronic alcoholism, weight loss
Symptoms of Refeeding syndrome Hypokalemia, hypophosphatemia and hypomagnesemia; cardiac arrhythmias, heart failure; acute respiratory failure
Hypophosphatemia In Refeeding syndrome: severe hemolysis, impaired cardiac function, - death
Hypomagnesemia In refeeding syndrome: tremor, muscle twitching, cardiac arrhythmias
Hypokalemia In refeeding syndrome: cardiac abnormalities
Thiamin In refeeding syndrome: Wernicke’s encephalopathy
Refeeding syndrome treatments Correct electrolyte abnormalities (via oral, enteral, parenteral route) before initiating nutrition support Administer volume and energy slowly Monitor pulse rate, intake and output, and electrolyte levels Provide appropriate vitamin supplementation A
Electrolytes BUN/Cr Albumin/prealbumin Ca++, PO4, Mg++ Weight Input/output Vital signs Stool frequency/consistency Abdominal examination Monitoring pt on EN
The suitability of a feeding formula should be evaluated based on Functional status of GI tract Physical characteristics of formula (osmolality, fiber content, caloric density, viscosity) Macronutrient ratios Digestion and absorption capability of patient Specific metabolic needs Contribution of the feeding to flui
Polymeric Formulas Contain intact macronutrients and require digestion
Oligomeric Formula Categorie Have hydrolyzed or partially hydrolyzed macronutrients facilitate digestion and absorption
Modular Formulas providing CHO, protein and fat as single nutrient to bump up one particular fraction
Lower Osmolality Large (intact) proteins Large starch molecules
Higher Osmolality Hydrolyzed protein or amino acids Disaccharides
Osmolar imbalance is caused by a gain or loss of water relative to a solute or a gain or loss of solute relative to water. <285 generally indicates water excess and >295 indicates water deficit.
HYDROLYZED FORMULAS 900 mOsm can create a hyperosmolar condition in the gut and contribute to excess fluid and e-lyte loss and diarrhea
Renal Solute Load: amount of nitrogenous waste and minerals that must be excreted by the kidney Is a measure of the particle concentration in feeding solution, which the kidneys must work to excrete. Contributed by protein and electrolyte composition
Common Indications for PN Nonfunctioning GI tract ultimate indication NPO for 5-7 days Patient has failed EN with appropriate tube placement Severe acute pancreatitis Severe short bowel syndrome Mesenteric ischemia Paralytic ileus Small bowel obstruction GI fistula un
Contraindications of PN Functional and accessible GI tract Patient is taking oral diet Prognosis does not warrant aggressive nutrition support (terminally ill) Risk exceeds benefit Patient expected to meet needs within 14 days
PN may be administered via peripheral access when Therapy is expected to be short term 7-14 days maximum Needs are greater than 5 days but less than 14 days Energy and protein needs are moderate Formulation osmolarity is <600-900 mOsm/L Frequent dressing change Fluid restriction is not necessary
Peripheral Limitations of PN Fluid tolerance Peripheral veins – low tolerance to concentrated solutions Fluid restricted patients – cardiopulmonary, renal, hepatic failure Not good candidates You will not be able to deliver adequate amounts of macronutrients in a very dilute s
Contraindications to Peripheral Parenteral Nutrition Significant malnutrition Severe metabolic stress Large nutrition or electrolyte needs (potassium is a strong vascular irritant) Fluid restriction Need for prolonged PN (>2 weeks) Renal or liver compromise
Monohydrous dextrose Source of carbs for PN
Crystalline amino acids— standard or specialty Source of Protein for PN
Safflower and/or soybean oil Source of Lipids in PN
Advantages of continuous PN Well tolerated by most patients Requires less manipulation decreased nursing time decreased potential for “touch” contamination
Disadvantages of continuous PN Persistent anabolic state altered insulin : glucagon ratios increased lipid storage by the liver Reduces mobility in ambulatory patients
Advantages of Cyclic PN Approximates normal physiology of intermittent feeding Maintains: Nitrogen balance Visceral proteins Ideal for ambulatory patients Allows normal activity Improves quality of life
Disadvantages of Cyclic PN Requires more nursing manipulation Increased potential for touch contamination Increased nursing time
Complications of PN Mechanical complications Pneumothorax, air embolism, blood clotting, catheter dislodgement Infection and sepsis Open port, catheter care Metabolic Complications Refeeding syndrome, electrolyte imbalances, hyperglycemia Gastrointestinal Complicat
Provide insulin with feedings or decrease dextrose how to manage Hyperglycemia Patients who are glucose intolerant or in severe metabolic stress inPN
Taper slowly How to manage Hypoglycemia When feedings are interrupted or discontinued in PN
Hypertriglyceridemia in PN Critically ill can’t tolerate lipid infusions Impaired lipid clearance
Refeeding in PN Re-feed slowly Life-threatening
Gallbladder disease in PN Parenteral for more than 4 weeks Sludge builds up, leading to gallstones Cholecystokinin injections or remove gallbladder
Monitoring and Evaluation: Complications for PN Standard monitoring protocols Intake and output Hyperglycemia Daily measures for electrolytes, BUN, creatinine, magnesium, phosphorus Lipid tolerance Complications similar to enteral nutrition GI complications Liver enzymes Infection
carbonic acid Aerobic respiration of glucose results in
lactic acid Anaerobic respiration of glucose results in
sulfuric acid oxidation of sulfur containing amino acids results in
acidic ketone bodies Incomplete oxidation of fatty acids results in
phosphoric acids Hydrolysis of phosphoproteins and nucleic acids
Carbonic acid - H2CO3 An intermediate step in the transport of CO2 and its removal from the body by gas exchange Converted to gaseous form and eliminated by the lungs Produced largest amount: 20,000mmol/day Major source of H+ ions
PaCO2 how carbonic acid is measured in the blood. It is considered a partial pressure.
Nonvolatile acids or fixed acids Produced as end products of metabolism of PRO, CHO, lipid can be organic or inorganic Can not be eliminated by the lungs
Kidney This organ Control amount of free H+ ions and amount of bicarbonate that is removed or retained, provides primary regulation of bicarbonate
Bicarbonate carbonic acid buffer system Primary ECF buffer against non carbonic acid changes
Protein buffer system Primary ICF buffer, also buffers ECF
Hemoglobin buffer system Primary buffer against carbonic acid changes
Phosphate buffer system Important urinary buffer, also buffers ICF
Phosphate buffer system Most important in the intracellular system Alternately switches Na+ with H+
Protein buffer system Behaves as a buffer in both plasma and cells Hemoglobin is by far the most important
Base When breathing is increased, the blood carbon dioxide level decreases and the blood becomes more
acidic When breathing is decreased, the blood carbon dioxide level increases and the blood becomes more
Chemosensitive areas This area of the respiratory center are able to detect blood concentration levels of CO2 and H+ Increases in CO2 and H+ stimulate the respiratory center The effect is to raise respiration rates
Hyperventilation in response to increased CO2 or H+ (low pH)
Hypoventilation in response to decreased CO2 or H+ (high pH)
Regulation by kidneys Control of alkaline - HCO3 Secretion of H+ into filtrate and reabsorption of HCO3- into ECF cause extracellular pH to increase HCO3- ( in filtrate reabsorbed Rate of H+ secretion increases as body fluid pH decreases Increased or decreased based on n
secreting or absorbing H+ or HCO3- controlling excretion of acids and bases generating additional buffers Renal mechanisms support buffer systems by:
Ammonia buffer system Tubular deamination creates NH3, which difuses into the tublule and buffers H+ by grabbing it and becoming NH4+ Bicarbonate is reabsorbed along with Na+
Acidosis physiological state resulting from abnormally low plasma pH
alkolosis physiological state resulting from abnormally high plasma pH
RESPIRATORY ACIDOSIS develops when the lungs don't expel CO2 adequately This can happen in diseases that severely affect the lungs, such as emphysema, chronic bronchitis, severe pneumonia, pulmonary edema, and asthma
Collapse of lung, Decreased gas exchange between pulmonary capillaries and air sacs of lungs, Decreased Respiration,Obstruction of air passages common causes of respiratory acidosis
Anxiety, emotional disturbances 2) Respiratory center lesions 3) Fever 4) Salicylate poisoning (overdose) 5) Assisted respiration 6) High altitude (low PO2) causes of respiratory alkolosis
METABOLIC ACIDOSIS Ingesting an acid or a substance that is metabolized to acid 2) Abnormal Metabolism 3) Kidney Insufficiencies 4) Strenuous Exercise 5) Severe Diarrhea
ketoacidosis Body metabolizes fat rather than glucose Accumulations of metabolic acids cause an increase in plasma H
Metabolic alkalosis A reduction in H+ in this case can be caused by a deficiency of non-carbonic acids This is associated with an increase in HCO3-
causes of metabolic alkalosis Ingestion of Alkaline Substances 2) Vomiting ( loss of HCl )
Created by: reihing25
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