Presentation on theme: "Alterations in Fluid, Electrolyte and Acid-Base Balance in Children Dr. Nataliya Haliyash, MD, BSN Institute of Nursing, TSMU."— Presentation transcript:
Alterations in Fluid, Electrolyte and Acid-Base Balance in Children Dr. Nataliya Haliyash, MD, BSN Institute of Nursing, TSMU
Pediatric Differences ECF/ICF ratio varies with age Neonates and infants have proportionately larger ECF volume Infants: high daily fluid requirement with little fluid reserve; this makes the infant vulnerable to dehydration.
Fluid Loss; Infants and <2yr. excretion is via the urine, feces, lungs and skin have greater daily fluid loss than older child more dependent upon adequate intake greater about of skin surface (BSA), therefore greater insensible loss. respiratory and metabolic rates are higher therefore, dehydrate more rapidly
Mechanism to Restore balance kidney: conserves water, regulates electrolyte excretion <2yr kidneys immature less able to conserve or excrete water and solutes effectively greater risk for acid/base imbalances Will use the SG norm:
Fluid Volume Imbalances Dehydration: loss of ECF fluid and sodium. Caused by: vomiting, diarrhea, hemorrhage, burns, NG suctioning and drainage loss, adrenal insufficiency. Manifested by wt loss, poor skin turgor, dry mucous memb., VS changes, sunken fontanel Dehydration that is not corrected will lead to hypovolemic shock and death. Fluid overload: excess ECF fluid and excess interstitial fluid volume with edema. Causes: fluid overload, CHF. Manifested by wt.gain, puffy face and extremities, enlarged liver.
Clinical Manifestations of Dehydration Depend on the degree of dehydration. Weight loss Rapid-thready pulse Hypotension Decreased peripheral circulation Decreased urinary output Increased specific gravity decreased skin turgor dry mucous membranes absence of tears a sunken fontanel in infants.
Nursing Considerations Nursing Considerations How can the nurse determine if the child is mildly dehydrated vs moderately dehydrated?
Mild Dehydration: Mild Dehydration: by history. hard to detect because the child may be alert, have moist mucous membranes and normal skin turgor. Wt loss may be up to 5% of body weight. The infant might be irritable; the older child might be thirsty vital signs will probably be normal Capillary refill will most likely be normal Urine output may be normal or sl less
Moderate Dehydration dry mucous membranes; delayed cap refill >2 sec; Wt loss 6-9% of body weight irritable, lethargic, unable to play, restless decreased urinary output: (in child >2yr) Sunken fontanel HR increased, BP decreased. Postural vital signs
Severe Dehydration wt loss > 10% body weight lethargic/comatose rapid weak pulse with BP low or undetectable; RR variable and labored. dry mucous membranes/parched; sunken fontanel decr or absent urinary output. Cap refill >4sec
Types of Dehydration and Sodium Loss Sodium may be: Low High Or normal
Isotonic Dehydration or Isonatremic Dehydration Loss of sodium and water are in proportion Most of fluid lost is from extracellular component Serum sodium is normal ( mEq/L) Harriet Lane Handbook, Most practitioners consider below 135 and above 148 a more conservative parameter ( ) Most common form of dehydration in young children from vomiting and diarrhea.
Hypotonic or Hyponatremic Dehydration Greater loss of sodium than water Serum sodium below normal Compensatory shift of fluids from extracellular to intracellular makes extracellular dehydration worse. Caused by severe and prolonged vomiting and diarrhea, burns, renal disease. Also by treatment of dehydration with IV fluids without electrolytes.
Hypertonic or Hypernatremic Dehydration Greater loss of water than sodium Serum sodium is elevated Compensatory shift from intracellular to extracellular which masks the severity of water loss (dehydration) delaying signs and symptoms until condition is quite serious. Caused by concentrated IV fluids or tube feedings.
Clinical Manifestations Associated with Degree of Dehydration
Dehydrated child Before… and after treatment
Nursing Diagnoses Nursing diagnoses appropriate for a child with dehydration may include: 1. Deficient fluid volume related to excessive fluid volume loss or inadequate fluid intake. 2. Risk for injury (fall) related to orthostatic (postural) hypotension. 3. Deficient knowledge (caregiver) related to lack of exposure to information about preventing/detecting dehydration.
Outcome Identification 1. The child will receive sufficient fluids to replace losses. 2. The child will exhibit signs of adequate hydration. 3. The child will not fall or sustain other injuries while hypotensive or lethargic. 4. Caregivers will demonstrate understanding of conditions that can lead to dehydration and of the early signs and symptoms.
Planning/Implementation Nursing interventions include: assessment of daily weight, vital signs, and maintenance of accurate intake and output records. Blood may be drawn to assess electrolytes, BUN and Creatinine levels administration of oral or IV fluids. Injury due to falls can be prevented by making sure that the side rails of the bed are raised, assessing level of consciousness, and monitoring the serum sodium level. An elevation in serum sodium will cause the brain cells to dehydrate and result in a loss of consciousness if not corrected quickly.
Diarrhea is increase in the number of stools and/or a decrease in their consistency as a result of malabsorption or alterations of water and electrolyte transport by the alimentary tract. Diarrhea may be acute or chronic.
Grades of diarrhea Mild diarrhea – 4 to 7 loose stools each day as a rule without other evidence of illness Moderate diarrhea – 8 to 15 loose or watery stooles daily with elevated temperature, vomiting, irritability, mild dehydration Severe diarrhea – numerous (>15) to continuous stools, evident signs of moderate to severe dehydration, drawn, flaccid expression, high pitched cry, irritable or lethargic or even comatose.
Acute gastroenteritis is characterized by the passage of ≥3 loose or watery stools in an 24 hour period, or the passage of one or more bloody stools, with or without vomiting, nausea, fever, and abdominal pain. Acute gastroenteritis usually refers to as an illness lasting no longer than days.
Pathogenesis of Acute Diarrhea Diarrhea results when the net intestinal fecal loss of fluid and salt exceeds the absorbed amount. There are 5 pathogenic forms of diarrhea: 1.Toxigenic diarrhea 2.Osmotic diarrhea 3.Secretory diarrhea 4.Invasive diarrhea 5.Motility disorders
Toxigenic diarrhea Toxins from bacteria, like enterotoxigenic E.coli or Vibrio cholerae, bind to specific receptors: labile toxin (LT) raises the level of cyclic guanosine monophosphate (cGMP) in the intestinal mucosa, stable toxin (ST) increases the adenasine 3 ׳ : 5 ׳ -cyclic monophosphate (cAMP) This leads to blocking the absorption of Na and Clˉ ions into the villous enterocytes. LT induce the secretion of Clˉ and HCO 3 ˉ ions by crypt cells.
Osmotic diarrhea Characterized by a positive osmotic gap of the stool Clinically, osmotic diarrhea is distinguished by the fact that the diarrhea diminishes when the patient fasts or stops eating the poorly ingested solute.
Secretory diarrhea There is no positive osmotic gap and the stool osmolality is equal to the ionic constituents: (Na + K) 2 = stool osmolality Food ingestion does not usually affect the stool volume The stool is watery without blood or pus and is characterized by very high volume and ion output
Invasive diarrhea Is caused by direct mucosal damage by the invasive organism It is similar to colitis and is usually associated with blood and mucous.
Motility disorders Hypermotility can cause diarrhea by reduction of contact time between intestinal mucosa and its contents, despite normal absorption function of the cell Hypomotility can be primary, as in idiopathic intestinal pseudo-obstruction syndrome, or secondary to neuronal disorders.
Clinical characteristics of infectious gastroenteritis in dependence on enteropathologic cause. OrganismCharacteristicsComments Rotavirus Incubation period:2-3 d. Abrupt onset Fever (≥ 38°C) for 48 hh Associated upper resp.tract infection Incidence higher in cool weather 6- to 24-month-old infants are more vulnerable Norwalk-like viruses Inc.period: 1-2 days Fever Loss of appetite Nausea/vomiting Abdominal pain Malaise Source of infection: drinking water, food Affects all ages Self-limited
Pathogenic Escherichia coli Incubation period: highly variable Diarrhea with moist-green, watery stool with mucus; becomes explosive Vomiting may be present from onset Abdominal distension Fever, intoxication Incidence higher in summer Usually interpersonal transmission, but may transmit via inanimate objects Salmonella groups (nontyphoidae) Salmonella groups (nontyphoidae) – gram- negative, non- encapsulated, nonsporulating Incubation period: 6 hh-21 day Rapid onset Variable symptoms – mild to severe Nausea, vomiting, and colicky abdominal pain followed by diarrhea, occasionally with blood and mucus Infants may be afebrile and nontoxic Highest incidence in children younger than 9 years, especially infants Transmission – via contaminated food and drink, more commonly poultry and eggs
Shigella groups Shigella groups – gram-negative, nonmotile, anaerobic bacilli Incubation period: 1-7 days Onset usually abrupt Fever (to 40.5°C) and cramping abdominal pain initially Febrile convulsions in 10 % cases Headache, neck rigidity, delirium Transmitted directly or indirectly from infected persons Vibrio cholerae groups Inc.period: 1-3 days Sudden onset of profuse, watery diarrhea without cramping, tenesmus, or anal irritation Stools are intermittemt at first, then almost continuous Stools are whitish, almost clear, with flecks of mucus – “rice water stools” Rare in infants Mortality is high Transmitted via contaminated food or water
Food poisoning: Staphylococcus Incub.period: 4-6 hours Nausea,vomiting Severe abdominal cramps Profuse diarrhea Shock may occur in severe cases May be a mild fever Transfered via contaminated food – inadequately cooked: custards, mayonnaise, cream-filled desserts Self-limited (24-72 hours) Exellent prognosis Botulism Clostridium botulinum Incub.period: 12 hr – 3 days Nausea,vomiting Diarrhea CNS symptoms with curare-like effect Dry mouth, dysphagia Transfered via contaminated food Variable severity – mild symptoms to rapidly fatal within a few hours Antitoxin administration
Diagnosis Diagnosis is based on: the history, physical exam, and laboratory studies focused on evaluating the child's hydration status and identifying the causative agent. The history should include the following data: Recent exposure to infectious agents Travel history Exposure to contaminated food and water supplies Exposure to turtles Attendance at a day-care center
If no systemic manifestations are present: Diagnostic laboratory tests are not indicated. Stool cultures should be performed for: children with a fever lasting more than 24 hours, blood or mucus in the stool, a family or household member with similar symptoms, or a positive stool white blood cell stain.
Treatment The main treatment aims are: To prevent dehydration – restoration and maintenance of adequate hydration and electrolyte balance. Nutritional support, adequate to prevent protracted diarrhea and malnutrition.
What about antimicrobial therapy? In about 30 % of patients no specific agent can be found Most of the isolated pathogenic organisms are viral The majority of the bacterial pathogens are self- limited In some cases, antimicrobial therapy prolongs the infection duration Antibiotic therapy has no effect on fluid transport nor on nutritional support
When should antibiotics be used? In young infants In immunocompromised patients When a systemic bacteremia is suspected. In case of specific persisting infection caused by Yersinia, Campylobacter, and Giardia
Rehydration In the majority of cases of acute diarrhea with mild or moderate dehydration, this aim can be achieved with oral rehydration solutions (ORS) 1-3 tsp of ORS every 10-15min to start (even if vomits some) 50ml/Kg/Hr is the goal for rehydration. Severe dehydration requires immediate admission to hospital and intravenous replacement of fluid and electrolytes.
The rationale for the use of ORS 1.During diarrhea, the normal mechanism for water and sodium absorption is impaired, so, the replacement of water or saline fluids alone will only lead to more diarrhea. 2.The sodium-glucose-coupled transport generally remains intact. This mechanism stimulates water transport by solvent drag.
The basic components of ORS Glucose Electrolytes in an isotonic solution. In the World Health Organization formula the glucose concentration is 2 %.
WHO recommendations for a sodium concentration 90 mEq/l, essentially for treatment of cholera mEq/l for countries, where cholera is not a concern and the stool sodium concentration in diarrheal illness is much lower mmol/l for neonates up to 2 mo whose kidneys have less capacity to excrete excess amounts of fluid and salt
Rehydration Fluids The World Health Organization recommends the following electrolyte concentrations for rehydration fluids: 20 g glucose/L, 90 mEq sodium/L, 80 mEq chloride/L, 20 mEq potassium/L, and 30 mEq bicarbonate/L. Encourage caregivers to look at product labels and make sure that the rehydration fluid they are choosing has the above electrolyte concentrations.
Composition of oral electrolyte solutions (in mEq/l) Na+K+ClˉOther anionCHO(%) WHO solution Gastrolyte Pedialyte Rehydralyte infalyte
Composition of “clear liquid” solutions Na+K+CHO(%) Pepsi Cola Coca Cola Root beer
Super-ORS Recent studies demonstrate the advantage of short glucose polymers as the carbohydrate source in ORS Traditionally it is widely used rice water % sugar syrup. Or carrot decoction: 500 g of cleansed carrot boil in 1 l of water during 1 hour, then mash it to homogenous mass and add boiled water up to 1 l. Boil for 10 min. Add 3 tsf of lemon juice. Give 1-2 teaspoon every 5-10 min up to 400 ml/day.
Why are drinks high in glucose avoided during rehydration? Simple sugars increases the osmotic effect in the intestine by pulling water into the colon, thereby increasing diarrhea and subsequent fluid/electrolyte loss Drinks high in glucose: apple juice, sodas, jello water.
Recommended foods during rehydration progression: In this question opinions differ: “bowel rest” versus “early feeding” is still controversial. Generally, formula feeding should be introduced gradually by starting with dilute mixtures.
In practice, refeeding can start gradually after 24 hr of only fluid intake, i.e.,”bowel rest”. An exception is made for nursing infants, who should continue their regular feeding. Children already on solid foods are easier to handle. Food with a high content of disaccharides and monosaccharides (fruits, sweets) should be withheld in the convalescent period. Foods with starch carbohydrates (cereal, rice, noodles, bananas, potatoes, carrot, cooked fruits & vegetables), soups, yogurt should be encouraged. It is important to give often small food-intakes (up to 8-10 times per day)
IV Therapy Used for severe dehydration or in the child who will not/cannot tolerate ORS Half 24hr maintenance plus replacement given within first 6-8hr (in ER) to rapidly expand the intravascular space. Usually a normal saline bolus. slower IV rate for the remainder of the first 24hrs nurse records IV vol infused hourly
Rehydration and IV solution Why is the child initially rehydrated with a normal saline bolus and not an IV solution with potassium? Potassium is only added to an IV after the patient has voided to avoid hyperkalemia in a child with little or no urinary output
Adding Potassium to Intravenous Solutions Be sure that the child is able to void (1 -2 ml/kg/hr) before adding potassium to the IV. Children who are dehydrated are oliguric and can become anuric. An anuric child will not be able to excrete electrolytes that are in the IV solution; therefore, if potassium is added to the IV, it would result in an elevated serum potassium. An elevated serum potassium can cause cardiac irritability and ventricular fibrillation. Always check the dose and dosage calculations prior to giving. Never give more than 40 mEq/L at a rate not to exceed 1 mEq/kg/hr. After adding potassium to an IV bag, shake it to make sure the potassium is equally distributed. Never give potassium by IV push.Never give potassium by IV push.
Which of the following IV solutions replaces Sodium? D5 W Lactated Ringers Normal Saline D5 ½ NS Answer: All but D5 WAnswer: All but D5 W
Calculation of intravenous fluid needs: maintenance For the 1st 10 Kg, replace at 100ml/Kg for the second 10 Kg, replace at 50ml/Kg for >20kg, replace at 20ml/Kg
Example of Maintenance Fluid Calculation Your patient is a 10 yr old weighing 35 Kg. You want to determine this patient’s 24hr maintenance fluid needs: for the first 10 Kg give 100ml/Kg = 1000ml for the second 10 Kg: 50ml/Kg = 500ml for the remaining 15 Kg (35-20Kg), replace at 20 ml/Kg: 20 15 = 300ml = 1800 ml/day.
How much fluid should this patient get per hour? 1800 ml / 24 hrs = 75 ml/hr. Therefore, if the patient was NPO and not taking in fluids from any other source, the IV should be running at 75ml/hr. If there is a deficit that also needs to be replaced, the IV rate may be slightly higher for a defined period of time. If the patient is receiving fluids from other sources, these need to be accounted as well
Practice Problems for Calculating 24hr Fluid Maintenance and the hourly IV rate for: A 9 yr old patient who weighs 20 Kg. A 6 mo old baby who weighs 8 Kg An 24mo old toddler who weighs 18 Kg A 3 yr old preschooler who weighs 28 Kg An 18 yr old who weighs 50 Kg
Answers for 24hr Fluid Calc. 9yr old wt 20 Kg = 1500 ml/day 6mo old wt 8Kg= 800 ml/day 36mo old wt 18 Kg= 1400 ml/day 3yr old wt 28Kg=1660 ml/day 18yr old wt 50Kg= 2100 ml/day Adult > 50Kg= 2-3 L/day
Clinical Assessment / Management of Edema assess dependent limbs if ambu or sacrum if lying ascites; periorbital edema; rings too tight pitting edema for degree of swelling daily wt and strictly In and Out elevation/change position Q2hr/ protect skin against breakdown distraction to deal with discomfort and limitations of edema.
Electrolyte Imbalances Electrolytes usually gained and lost in relatively equal amounts to maintain balance Imbalance caused by: Abnormal route of loss (vomiting/diarrhea) can disturb electrolyte balance Disproportionate IV supplementation Disease states: renal dis.
Hypernatremia Excess serum sodium in relation to water Causes: Too concentrated infant formula Not enough water intake Clinical manif.: thirst, lethargy, confusion Seizures occur when rapid or is severe. SG concentrated Lab test: serum sodium Treatment: hypotonic IV solution
Hyponatremia Excess water in relation to serum sodium Most common sodium imbalance in children Causes: Infants vulnerable to water intoxication:dilute form, excess pool water, poorly developed thirst mech so cont to drink and can’t excrete excess water.
Hyponatremia (cont) Clinical manif: decreased level of consciousness d/t swelling of brain cells. Anorexia, headache, muscle weakness, decreased DTR’s, lethargy, confusion or coma. Seizures occur when rapid or severe. SG dilute: Lab tests: serum sodium Treatment: hypertonic solution.
Hyperkalemia Excess serum potassium Causes: excess K intake from IV overload, blood transfusion, rapid cell death (hemolytic crisis, large tumor destruction from chemo rx, massive trauma, metabolic acidosis from prolonged diarrhea and in DM when insulin levels are low Insulin drives K back into the cells decreased K loss from Renal insufficiency
Hyperkalemia (cont) Clinical manif: all are related to muscle dysfunction: hyperactivitiy of GI smooth muscle: intestinal cramping and diarrhea. Weak skeletal muscles Lethargy Cardiac arrhythmias (tachycardia, prolonged QRS, peaked T waves: also AV block and VTach). Lab test: serum potassium Treatment: correct underlying condition (take K out of the IV) dialysis (peritoneal or hemo), Kayexalate (po or enema), K wasting diuretics, IV calcium, bicarbonate, insulin and glucose. Low potassium diet.
Hypokalemia Decreased serum potassium Causes: diarrhea and vomiting, ingestion of large amts black licorice, diuretics, osmotic diuresis (glucose in urine as in DM), NPO without K replacement in IV, NG Sx, bulimia, insulin. Also in nephrotic syndrome, cirrhosis, Cushing Syndrome, CHF (to be covered elsewhere)
Hypokalemia (cont) Clinical manif: muscle dysfunction Slowed GI smooth muscle resulting in abdominal distention, constipation and paralytic ileus Skeletal muscles are weak; may effect respiratory muscles Cardiac arrhythmias: hypokalemia potentiates Digitoxin Toxicity. Lab test: serum potassium Treatment: oral and/or IV potassium, diet rich in K.
Hypercalcemia Excess calcium Needs vit D for efficient absorption; most of Ca is stored in the bones. Causes: bone tumors that cause bone destruction, chemo rx release Ca from the bones; immobilization causes loss from the bones (usually excreted) but if kidneys can’t clear it, hypercalcemia results, increased intake (milk-alkali syndrome).
Hypercalcemia (cont) Clinical manif: Ca imbalances alter neuromuscular irritability with non-specific symptoms Constipation, anorexia, N/V, fatigue, skeletal muscle weakness, confusion, lethargy. Renal calculi, cardiac arrhythmias HyperCa increases Na and K excretion leading to polyuria and polydipsia. Rx: serum Ca, Ionized Ca, fluids, Lasix, steroids, dialysis.
Hypocalcemia Decreased serum calcium Causes: decreased intake of Ca and/or Vit D (adolescents are vulnerable d/t fad diets and the deficit cannot be made up later, increasing risk for osteoporosis). Limited exposure to sunlight, premature infants and dark skinned people at increased risk to inadeq. Vit D and therefore decreased Ca absorption. Parathyroid dysfunction, multiple transfusion (Citrate binds Calcium), steatorrhea (as in pancreatitis and Cystic Fibrosis) binds Calcium in the stool.
Hypocalcemia (cont) Clinical Manif:acute situation related to increased muscular excitability: tetany. +Chvostek’s Sx, + Trousseau’s Sx. In children: Twitching, cramping, tingling around the mouth or fingers, carpal/pedal spasms. In infants: tremors, muscle twitches, brief tonic-clonic seizures, CHF. Laryngospasm, seizures and cardiac arrhythmias in severe situations. Chvostek’s Sx: tap the skin lightly in front of the ear (over the facial nerve), if the corner of the mouth draws up, d/t muscular contraction = +Chvostek’s Sx. Trousseau’s Sx: + if carpal spasm after BP cuff inflated ~ 3min.
Hypocalcemia (cont 2) In children and adolescents, chronic hypocalcemia more common, manif. By spontaneous fractures. Lab tests: serum Ca; bone density study Rx: oral and/or IV Ca, Ca rich diet
Hypermagnesemia Excess in Mg. Imbalances characterized by neuromuscular irritability Causes: impaired renal function, Mag Sulfate given perinatally to treat eclampsia, increased use of laxatives, enemas, antacids, IV fluid additives.
Hypomagnesemia Decreased serum Mg. Stored in cells and bones Causes: prolonged NPO without replacement, chronic malnutrition, chronic diarrhea, short bowel syndrome, malabsorption syndromes, steatorrhea, multiple transfusions, prolonged NG Sx, some medications.
Hypomagnesemia (cont) Clinical manif: increased neuromuscular excitability (tetany). Hyperactive reflexes, skeletal muscle cramps, twitching, tremors, cardiac arrhythmias, seizures. Lab: serum Mg along with Ca and K. Rx: po/IV Magnesium admin and treating underlying cause of imbalance.
Critical Thinking: Clinical Evaluation of Fluid and Electrolyte Imbalance How can you evaluate children appropriately for fluid and electrolyte imbalance without thinking through the clinical manifestations of every possible disorder, one after the other?
Answer to Critical Thinking: 3 paragraphs of text that review this concept and pull the content together with clinical application: 1) risk factor assessment 2) exam several body systems: cardiovascular, respiratory, neurological 3) look for factors that alter intake, retention, and loss of fluids and electrolytes 4) consider growth and development to realize problems most common to the age group. 5) clinical assessment: wt, fluid balance, vascular volume (BP, HR), interstitial volume (edema?), mentation, DTR’s, muscle irritability, GI function, cardiac rhythm, assess electrolyte levels.
Fluid and Electrolyte Worksheet Use the fluid and electrolyte worksheet to help review some of the major concepts of fluid and electrolyte imbalance.
pH - Is the acidity or alkalinity of a solution. pouvoir hydrogène - From French pouvoir hydrogène ("hydrogen power“) - pH is the Hydrogen ion concentration [H+] of a solution. - It is a measure of the solution's acidity. pH is defined as the negative logarithm of the concentration of H+ ions: pH = -log 10 [H+]
The greater the concentration of H +, the more acidic a solution is. The lower the concentration of H +, the more basic or alkaline a solution becomes. Neutral AcidicAlkaline 7114
Neutral H+H+ HCO 3 - Alkaline Acidic
Acid Base Balance normal arterial blood pH: (in general) Acidosis < 7.35 : too much acid Alkalotic > 7.43 : too little acid pCO2 reflects carbonic acid status: 40 mmHg (+- 5) HCO3- reflects metabolic acid status: 24 mmol/l (+- 4)
Respiratory Acidosis caused by decr respir effort build up of CO2 in the blood pH decr or normal; pCO2 incr. Symptoms manifested: confusion, lethargy, HA, incr ICP, coma, tachycardia, arrhythmias
Management of Respiratory Acidosis Incr ventilatory rate give O2 intubate adm NaHCO3
Clinical Conditions that cause Respir Acidosis conditions associated with decreased respiratory drive, impaired gas exchange/air trapping, ie: head trauma, general anesthesia, drug overdose, brain tumor, sleep apnea, mechanical under ventilation, asthma, croup/epiglottitis, CF, atelectasis, MD, pneumothorax.
Respiratory Alkalosis caused by hyperventilation CO2 is being blown off pH incr : pCo2 decr Symptoms: dizziness, confusion, neuromuscular irritability, paresthesias in extremities and circumoral, muscle cramping, carpal or pedal spasms.
Management of Resp. Alkalosis First determine if oxygenation is adequate, if not, you don’t want to slow the RR. Determine the cause and correct it: Causes of hypervent: hypoxemia, anxiety, pain, fever, ASA toxicity, meningitis/encephalitis, Gram - sepsis, mechanical overventilation. Ipecac is no longer recommended for treatment of ingestions.
Metabolic Acidosis caused by a loss of bicarbonate (HCO3) therefore, is an incr of acids in the blood pH decr or moving towards normal pCo2 decr ; HCO3 decr Symptoms: Kussmaul respirations = incr rate and depth as compensation (hyperventilation / acetone breath), confusion, hypotension, tissue hypoxia, cardiac arrhythmias, pulmonary edema.
Management of Metabolic Acidosis Identify and treat underlying cause In severe case may give IV NaHCO3 to incr pH, or insulin/glucose. Causes of MA for gain of acid: ingestion of ASA, antifreeze, oliguria, RF, HAL, DKA, starvation or ETOH KA, lactic acidosis (tissue hypoxia). Loss of HCO3: maple syrup urine disease, diarrhea, RF.
Metabolic Alkalosis caused by loss of H+ or HCO3 retention HCO3 incr with probable incr in pH, incr pCO2. Symptoms:weak, dizzy, muscle cramps, twitching, tremors, slow shallow resp., disorientation, seizures.
Management of Metabolic Alkalosis correct underlying cause; facilitate renal excretion of HCO3. admin NS, K+ if hypokalemic, replace loss of fluids, prec for Sz, monitor I and O and electrolytes Causes: prolonged vomiting, ingestion of lg quantities of bicarb, antacids, loss of NG fluids, hypokalemia from prolonged diuretic use, multiple blood transfusion with citrate.
ABG Basic (Uncompensated) Analysis Resp Acidosis: low pH and high PaCO2 Resp Alkalosis: incr pH and low PaCO2 Metab Acidosis: low pH and nl PaCo2; decr HCO3 Metab Alkalosis: high pH; nl PaCO2 ; high HCO3
ABG Analysis with Compensation Resp Acidosis: HCO3 will incr, pH will approach nl; PaCO2 will still be increased Resp Alkalosis: HCO3 will decr, pH will approach nl; PaCO2 will still be decreased Metab Acidosis: PaCO2 will decr, pH will approach nl; HCO3 will still be decreased Metab Alkalosis: PaCO2 will incr, pH will approach nl; HCO3 will still be increased