AGRAWAL Fluid Electrolytes Children National

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AGRAWAL Fluid Electrolytes Children National Powered By Docstoc
					Fluid & Electrolytes
 Maintenance & Dehydration,
    Sodium & Potassium
    Acid-Base Disorders
       Dewesh Agrawal, MD
         Assistant Professor
  Pediatrics & Emergency Medicine
Learning Objectives
 Understand the composition of body fluids and
  maintenance fluid & electrolyte requirements
 Describe the appropriate fluid management of
 Recognize the common etiologies, presentations, and
  complications associated with the management of
  hyponatremia and hypernatremia
 Recognize the common presentations, etiologies and
  management of hyperkalemia and hypokalemia
 Describe common etiologies and a diagnostic scheme for
  acid-base disturbances
          Question #1
Which of the following statements is correct regarding the
composition of body fluids in children?
A. The percentage of total body water (TBW) does not
   change with age
B. Extracellular fluid (ECF) volume drops precipitously
   after birth
C. Two-thirds of total body water (TBW) is made up of
   extracellular fluid (ECF) in older children
D. One-quarter of extracellular fluid (ECF) is interstitial
   fluid (IF) and three-quarters is plasma volume (PV)
E. Intracellular fluid (ICF) is high in sodium and
   chloride and extracellular fluid (ECF) is high in
   potassium and phosphate
Body Fluid Composition
 TBW as a percentage of body
  weight decreases with age
 TBW = ICF (2/3) + ECF (1/3)
    ECF = IF (3/4) + PV (1/4)
 For a 3-year-old weighing 18 kg:
    TBW = 12L (2/3 body weight)
       ICF = 8L
       ECF = 4L
           (IF = 3L, PV = 1L)
Body Fluid Composition

  (mEq/L)   ICF      ECF
  Na+        15      140
  K+        140        4
  Cl-         3      105
  HCO3-      10       24
  PO43-     110        2
           Question #2
A 10-year-old boy has gastroenteritis with bloody diarrhea
and has had no urine output over the past 24 hours.
Findings include lethargy, BP 85/50, HR 140, capillary refill
>4 seconds, mottled skin, Na 132, K 5.0, Cl 100, HCO3 12,
BUN 100 mg/dL, Cr 10 mg/dL, hemoglobin 12 g/dL, and
platelets 70 (x103/mm3). The most appropriate INITIAL
parental fluid regimen is to:
A. Administer a 20 mL/kg bolus of NS
B. Administer maintenance fluids
C. Administer maintenance fluids plus replace GI
D. Restrict fluids to insensible water losses
E. Restrict fluids to insensible water losses plus
   ongoing urine and GI losses
Fluid Resuscitation Therapy
 Always initially use an isotonic crystalloid solution (NS or
  LR) to rehydrate
    Patient has compensated, hypovolemic shock from dehydration
    Most acute fluid losses in dehydration occur from the ECF
    Because patient has renal failure, should not bolus with LR (K+ 4
 Give three 20 mL/kg boluses (each over 20-60 minutes)
  of crystalloid before considering colloids (albumin,
  PRBC’s, whole blood, FFP)
 Even thought the patient has renal failure, the goal of
  fluid resuscitation therapy is the same: restoration of
  intravascular volume
    After intravascular volume has been restored, then further fluid
     management will likely require fluid restriction given patient’s
     potential anuric status.
    Maintenance fluids should then be restricted to insensible losses
     and ongoing losses (urine output and GI losses)
Composition of Standard IVF

Solution       Dextose     Na+       K+        Cl-      HCO3-      Osmolality
                (g/dL)   (mEq/L)   (mEq/L)   (mEq/L)   (mEq/L)     (mOsm/L)
D5W              5         0         0         0          0           278

NS (0.9%)        0        154        0        154         0           308

D5 ½NS           5         77        0         77         0           432
D5 ¼NS           5         34        0         34         0           346
Lactated         0        130        4        109         28          275
Ringers (LR)                                           (lactate)
           Question #3
Which of the following statements is correct
regarding the use of oral rehydration solutions in
the management of acute pediatric gastroenteritits?
A. Enteral feedings are initiated following 24 hours of
   bowel rest and IVF
B. Carbohydrates are predominantly absorbed in the
C. Deficit fluid and electrolytes are replaced via
   sodium-glucose cotransporter in the small intestine
D. High sodium concentrations allow for replacement of
   total body sodium deficiency
E. Hyperosmolar solutions containing complex
   carbohydrates are usually required
Oral Rehydration Therapy
 No need for bowel rest
 Avoid excessive carbohydrate concentrations
    Carbohydrate contents of around 2 g/dL appear to be optimal for
     sodium absorption in the small intestine
 Pedialyte (250 mOsm/L)
 Contraindications:
      Severe dehydration
      Intractable vomiting
      Shock or impending shock
      Lack of personnel
 Goal over 4 hours:
    Mild: 40-60 mL/kg
    Moderate: 60-90 mL/kg
Dehydration & Sodium
 In general, the more acute the dehydration,
  the more that fluid losses are from the ECF
   As additional time (days) elapse, more fluid is
    lost from the ICF as well
 Thus, most acutely dehydrated children
  have lost large amounts of Na+ and Cl- with
  their fluid losses
   Rationale for bolusing with NS or LR
Sodium Homeostasis
 Sodium is unique among electrolytes because
  water balance, not sodium balance, usually
  determines its concentration
    Disorders of sodium homeostasis are usually
     a result of disturbed water balance
       Too much water: hyponatremia
       Too little water: hypernatremia
    Disorders of sodium balance often lead to
     disordered water homeostasis
       Too much sodium: fluid overload (edema)
Sodium Homeostasis
 Anti-diuretic hormone (ADH):
   Promotes renal water reabsorption in
    response to volume depletion and
    hyperosmolarity (hypernatremia)

 Renin-Angiotensin-Aldosterone system:
   Promotes renal Na+ (and fluid) reabsorption in
    response to volume depletion
 [Na+] < 130 mEq/L
 Symptoms:
   Depend on absolute [Na+] along with rapidity of
   Nonspecific symptoms related to CNS effects:
      Mild (125-130 mEq/L): generally asymptomatic
      Moderate (120-125 mEq/L): nausea, headache,
       fussiness/agitation, malaise, weakness,
      Severe (<120 mEq/L): lethargy, confusion,
       pyschosis, seizures, coma, respiratory
       depression, cerebral edema/herniation, death
 “Factitious/Dilutional” Hyponatremia:
    Patient’s serum is usually hypertonic (POsm>290)
    Results from presence of impermeable solutes other
     than Na+, such as glucose or mannitol
    For every 100 mg/dL elevation of serum glucose,
     serum Na+ decreases by 1.6 mEq/L
 Pseudohyponatremia:
    Patient’s serum is usually isotonic (POsm= 275-290)
    Results from increase in nonaqueous portion of serum
     (usually 7%):
        Severe hyperlipidemia/hypertriglyceridemia
        Severe hyperproteinemia
 True hyponatremia:
    Patient’s serum is usually hypotonic (POsm<275)
    Key is to determine the patient’s total body volume
     status and measure urine [Na+] and osmolality
Plasma Osmolality

Posm = (2 x [Na+]) + (Glucose/18) + (BUN/2.8)
          (mEq/L)     (mg/dL)        (mg/dL)
Hyponatremia: Diagnostic Algorithm


                        Psuedohyponatremia        Hypotonic
                         (hyperlipidemia or    True Hyponatremia

              Hypovolemic                       Euvolemic                    Hypervolemic

                                              Endocrine Causes
Extrarenal Losses          Renal Losses        Urine Na>20mEq/L    Edematous States    Renal Failure
Urine Na<20mEq/L        Urine Na>20mEq/L      Water Intoxication   Urine Na<20mEq/L   Urine Na>20mEq/L
                                                Urine Osm<100
True Hyponatremia
 Hypovolemic: (Urine osm > 100 mOsm/L)
    Extrarenal losses (Urine Na+ < 20 mEq/L): vomiting, diarrhea,
     excessive sweating, hemorrhage, distributive shock
    Renal losses (Urine Na+ > 20 mEq/L): diuretic use,
     mineralcorticoid deficiency, salt-losing nephropathy, cerebral salt
 Euvolemic:
    Urine osm > 100 mOsm/L: SIADH, glucocorticoid deficiency,
     hypothyroidism (endocrine causes)
    Urine osm < 100 mOsm/L: free H2O intoxication (psychogenic
     polydipsia, beer-drinker’s potomania, accidental, near-drowning)
 Hypervolemic:
    Edematous states with decreased effective circulating volume
     (Urine Na+ < 20 mEq/L): CHF, cirrhosis, nephrotic syndrome
    Renal Failure (Urine Na+ > 20 mEq/L)
         Question #4
An 11-month-old girl is brought to the emergency
department because of a new-onset, generalized seizure.
She has been playing all day in a backyard pool. There is
no history of fever or trauma, and her development has
been normal. Which of the following tests will MOST likely
explain the patient’s presentation?
A.   Culture of the cerebrospinal fluid
B.   Magnetic resonance imaging of the brain
C.   Skull radiography
D.   Computed tomography of the head
E.   Serum electrolyte concentrations
          Question #5
The patient’s serum sodium concentration is 118 mEq/L.
There is no response of the generalized seizures to the
administration of appropriate doses of lorazepam,
phenobarbital, and fosphenytoin. Which of the following is
the MOST appropriate next step in the management of this

A.   Emergent consultation with a pediatric neurologist
B.   Emergent consultation with a pediatric nephrologist
C.   Furosemide 1 mg/kg IV
D.   5 mL/kg bolus of 3% (hypertonic) saline
E.   10 mL/kg bolus of D5 ½NS
        Question #6
A 5-year-old child is brought to the emergency
department with new-onset, generalized seizures.
Results of laboratory evaluation include Na 118, K
4, Cl 95, HCO3 20, BUN 11, Cr 0.5, glucose 90,
UNa 50, UK 20, and UOsm 500. Which of the
following is the MOST likely explanation for these
A. Acute renal failure
B. Addison disease
C. Congestive heart failure
D. Hyponatremic dehydration
Syndrome of Inappropriate Antidiuretic
Hormone Secretion (SIADH)
 Definition: Inappropriately concentrated urine (>100
  mOsm/L) in the setting of true, euvolemic
      Dilute serum: Posm < 275 mOsm/L; [Na+] < 130 mEq/L
      Clinical euvolemia
      Inappropriately concentrated urine (Uosm > 100 mOsm/L)
      Elevated urine sodium (UNa > 20 mEq/L)
 Etiology:
      CNS disease (meningitis, infection, trauma)
      Pulmonary disease (pneumonia, bronchiolitis, PPV, COPD)
      Malignancy (CNS, pulmonary, pancreatric, leukemia)
      Pharmacologic (carbamazepine, DDAVP, cyclophosphamide,
       phenothiazines, tricyclic antidepressants, SSRI’s, ACE
          Question #7
On the second day of hospitalization, a 5-year-old child who
has pneumococcal meningitis develops a serum sodium
concentration of 122 mEq/L. Examination reveals an awake
and responsive child whose weight is 20 kg (an increase of
1 kg from admission), T 37.8, BP 100/60, and HR 100. The
MOST appropriate management of this patient’s fluid status
is to:
A.   Administer demeclocycline
B.   Infuse D5 1/3 NS at maintenance rate
C.   Infuse 5 mL/kg hypertonic (3%) saline bolus
D.   Infuse NS at maintenance rate
E.   Restriction of fluids
          Question #8
A 16-month-old boy has had severe emesis and diarrhea for
3 days. On examination he appears dehydrated. You
administer fluids rapidly to correct his volume and serum
electrolyte abnormalities. On the next day, he appears
confused and exhibits quadriparesis and dysarthria. MRI
imaging reveals demyelination of the central pons. Of the
following, the rapid correction of which condition is MOST
likely responsible for these findings?
A.   Hyperkalemia
B.   Metabolic acidosis
C.   Hypernatremia
D.   Hyponatremia
E.   Hypocalcemia
 [Na+] > 150 mEq/L
 Symptoms: Depend on absolute [Na+] along with
  rapidity of increase
    ECF and plasma volume are preserved even in the
     setting of very severe dehydration
    Infants:
       Lethargy, irritability, “high-pitched” cry, “doughy” skin,
    Older patients:
       Nonspecific symptoms related to CNS effects &
       Weakness, listlessness, agitation, irritability, mental status
       CNS thrombosis and/or hemorrhage
 Etiology:
    Primary water deficit: excessive loss of body water (that is greater
      than the loss in sodium)
         Gastroenteritis with hypernatremic dehydation
         Osmotic diuresis (diabetes mellitus, mannitol therapy)
         Diabetes insipidus
         Increased insensible water losses (premature infants, burns)
         Inadequate access to free water (inadequate breast feeding,
          intentional or uninententional withholding of water intake)
         Primary hypodipsia (defective thirst mechanism)
     Primary sodium excess: excessive gain of sodium
         Iatrogenic (improperly mixed formulas or rehydration solutions),
          excessive NaHCO3 or hypertonic saline during resuscitation,
          hypernatremic enemas)
         Intentional salt poisoning (Munchausen by proxy)
         Ingestion of sea water
            Question #9
A previously healthy 1-month-old girl presents with
lethargy. Findings include no signs of dehydration, BP
90/60, HR 130. Laboratory evaluation reveals Na 174, K
5.5, Cl 138, HCO3 18, BUN 10, Cr 0.2, glucose 150.
Urine Na is 140 mEq/L. The infant is exclusively formula
fed. The MOST likely etiology of this patient’s
hypernatremia is:
A.   Central diabetes insipidus
B.   Nephrogenic diabetes insipidus
C.   Incorrect mixing of the formula
D.   Hypernatremic dehydration
           Question #10
A 5-year-old boy is hospitalized following a motor vehicle
accident. Evaluation reveals a displaced femur fracture,
depressed skull fracture, and cerebral edema. He develops
polyuria postoperatively in the ICU. You decide to measure
serum and urine sodium as well as urine osmolality. Of the
following, the findings that are MOST consistent with the
diagnosis of diabetes insipidus are:

A.   SNa 120 mEq/L, UNa 10 mEq/L, UOsm 600 mOsm/L
B.   SNa 120 mEq/L, UNa 50 mEq/L, UOsm 300 mOsm/L
C.   SNa 140 mEq/L, UNa 20 mEq/L, UOsm 300 mOsm/L
D.   SNa 160 mEq/L, UNa 10 mEq/L, UOsm 600 mOsm/L
E.   SNa 160 mEq/L, UNa 10 mEq/L, UOsm 100 mOsm/L
Diabetes Insipidus
 Physiology:
    Without ADH, the urine becomes very dilute (approaching 100
     mOsm/L) and excess free water is excreted, despite
     intravascular volume depletion, leading to hypernatremia
 Etiology:
    Central DI: absence of ADH secretion
       CNS tumors, CNS herniation, encephalitis, head trauma,
    Nephrogenic DI: end-organ resistance to action of ADH
       Pharmaceuticals (demeclocyline, lithium, clozapine),
        severe hypercalcemia or hypokalemia, defective tubular
        ADH receptor
 Signs/Symptoms:
    Irritability, polydipsia, polyuria, hypernatremic dehydration
            Question #11
A 3-month-old infant has had diarrhea and lethargy for 4
days. Findings include BP 80/40, HR 150, doughy skin and
sunken eyes. Laboratory evaluation reveals Na 170, K 5.6,
Cl 132, HCO3 15, BUN 60, Cr 1.0, glucose 160. Fluid
therapy is instituted, and 12 hours later, the patient has a
generalized seizure. The MOST likely explanation for the
seizure is:
A.   Rapid correction of hypernatremia
B.   Rapid correction of metabolic acidosis
C.   Rapid correction of hyperglycemia
D.   Idiopathic epilepsy
E.   Hyperkalemia
Hypernatremic Dehydration
 With time (48-72 hours), the initial brain cellular
  dehydration induced by the hypertonic ECF and
  movement of fluid from brain cells to the ECF will
  resolve with the generation of “idiogenic”
  osmoles in brain cells
 Hypernatremic that is corrected too rapidly may
  lead to cerebral edema and secondary seizures
  because these “idiogenic osmoles” will induce
  the rapid movement of fluid into brain cells
 Goal is to correct the serum [Na+] very slowly,
  not more than 8-12 mEq/L per day
Potassium Homeostasis
 Extracellular-Intracellular shifts:
    Na/K ATP-ase:
        About ½ of a given potassium load is translocated into cells
         (primarily liver and muscle)
        Insulin and epinephrine (via beta-adrenergic receptors) regulate this
         process via stimulation of the Na/K ATP-ase
    Acid-base balance:
        Systemic acidosis: results in movement of K+ out of cells
        Systemic alkalosis: results in movement of K+ into cells
             For every 0.1 unit change in blood pH, plasma [K+] changes on average
              0.6 mEq/L (range 0.3-1.3 mEq/L) in the opposite direction
 Kidney:
    Aldosterone:
        Stimulates renal K+ excretion
    Acid-base status:
        Acidosis: inhibits tubular K+ secretion
        Alkalosis: stimulates tubular K+ secretion
    Diuretics:
        Promote renal K+ excretion by increasing tubular flow rate and
         increasing tubular [Na+]
         Question #12
A 10-day-old baby boy presents with seizures. He has had
poor feeding for the past 2 days and vomiting, but no fever.
On exam, the infant has darkly pigmented scrotum and
nipples. Father reports that the infant is “extremely well-
endowed,” taking after himself. Laboratory evaluation
reveals Na 110, K 7.4, Cl 93, HCO3 9, BUN 16, Cr 0.4,
glucose 18 mg/dL. Which of the following is the MOST
likely diagnosis?
 A.   Type I RTA
 B.   Type II RTA
 C.   Pyloric stenosis
 D.   Congenital adrenal hyperplasia
 [K+] > 5.5 mEq/L
 Symptoms:
    [K+] > 7 mEq/L: weakness,
    [K+] > 9 mEq/L: tetany
 EKG signs:                           8.0
    [K+] ~ 7 mEq/L: peaked T-waves
    [K+] ~ 8 mEq/L: QRS widening,
       AV block
    [K+] ~ 9 mEq/L: ST depression,
       loss of P wave
    [K+] ~ 10 mEq/L: sine-wave QRS-   9.0
       T, bradycardia, ventricular
       dysrhythmias, cardiac arrest
 Spurious laboratory value:
    Hemolyzed sample, severe leukocytosis or thrombocytosis
 Increased intake:
    IV, PO, blood transfusion
 Transcellular shifts:
    Acidemia, rhabdomyolysis, tumor lysis syndrome, tissue necrosis,
     crush injury, intravascular hemolysis, malignant hyperthermia,
     medications (succinylcholine, digitalis, B-blockers)
 Decreased excretion:
    Renal failure, adrenal insufficiency, medications (ACE-inhibitors,
     Angiotensin II blockers, K-sparing diuretics, NSAIDs)
          Question #13
A 16-year-old adolescent female with history of
hypertension and chronic renal insufficiency from
lupus nephritis presents with dizzyness, weakness
and paresthesias. Medications include enalapril
and indomethacin. EKG shows peaked T-waves
and QRS widening. The MOST appropriate next
step in the management of this patient is:
A.   Initiation of hemodialysis
B.   Administer calcium gluconate IV
C.   Administer Kayexalate PO/PR
D.   Administer insulin (regular) 0.1 U/kg IV
E.   Elimination of dietary K+
 Treatment:
   Obtain EKG, place on cardiac monitor
   Normal EKG ([K+]<7):
      Eliminate K+ from diet and IV fluids
      Kayexalate 1 gm/kg PO/PR
   Abnormal EKG ([K+]>7):
      1st:
          Calcium gluconate 10% 50-100 mg/kg (0.5-1 mL/kg) IV or
           calcium chloride 10% 20 mg/kg (0.2 mL/kg) IV
      Then:
          NaHCO3 1-2 mEq/kg IV
          Regular insulin 0.1 U/kg IV with Dextrose 0.5-1 gm/kg
           (2-4 mL/kg of D25 or 5-10 mL/kg of D10)
          Consider dialysis
         Question #14
A 15-year-old adolescent female presents with weakness,
dizzyness, and recent 20 pound weight loss. She states her
appetite is good. She denies use of laxatives. Laboratory
evaluation reveals Na 135, K 2.5, Cl 80, HCO3 38, BUN 14,
Cr 0.6, glucose 98. HR is 65, and BP is 109/56. EKG has a
prolonged QT interval. What is the MOST likely diagnosis?
A.   Hyperthyroidism
B.   Bulimia nervosa
C.   Anorexia nervosa
D.   Addison disease
E.   Cushing syndrome
 [K+] < 3.5 mEq/L

 Symptoms:
      Skeletal muscle: weakness, paralysis, and/or cramps
      Smooth muscle: GI ileus/constipation, urinary retention
      CNS: apathy
      Kidney: nephrogenic diabetes insipidus and secondary polydipsia

 EKG signs:
    QT prolongation, flattened/absent T-waves, U waves, ST depression
 Decreased intake
 Extra-renal losses:
    Vomiting, diarrhea, laxative abuse, excessive sweating
 Renal losses:
    With metabolic acidosis: RTA (Types I or II), DKA
    With metabolic alkalosis: diuretics (loop and thiazide), Bartter
     syndrome, Gitelman syndrome, hyperaldosteronism, Cushing
     syndrome, Liddle syndrome
    Other: tubular toxins (amphotericin, cisplatin, aminoglycosides),
     hypomagnesemia, postobstructive diuresis
 Transcellular shifts:
    Alkalemia, medications (insulin, beta-agonists, theophylline,
     caffeine), hyperthyroidism, familial hypokalemic periodic paralysis
Acid-Base Disturbances

  H+ + HCO3-  H2CO3  H2O + CO2
    Kidney               Lungs
  (Metabolic)         (Respiratory)
Acid-Base Disturbances
Three Step Approach:

  1. What is the pH?
        If pH < 7.4, then primary acidosis
        If pH > 7.4, then primary alkalosis

  2. Is the primary disturbance metabolic or respiratory?
        Primary acidosis (pH < 7.4):
            If HCO3 < 24, then primary metabolic acidosis
            If pCO2 > 40, then primary respiratory acidosis
        Primary alkalosis (pH > 7.4):
            If HCO3 > 24, then primary metabolic alkalosis
            If pCO2 < 40, then primary respiratory alkalosis

  3. Is there a compensatory acid-base disturbance?
        HCO3 and pCO2 will move in the same direction
            either both high or both low
Acid-Base Disturbances


           pH < 7.4                               pH > 7.4
       Primary Acidosis                       Primary Alkalosis

 HCO3 < 24          pCO2 > 40          HCO3 > 24           pCO2 < 40
  Primary            Primary            Primary             Primary
 Metabolic          Respiratory        Metabolic           Respiratory
  Acidosis           Acidosis           Alkalosis           Alkalosis
Acid-Base Disturbances
 Primary (Pure) Metabolic Disturbances:

   pH:      7.0    7.1   7.2 7.3 7.4         7.5   7.6
   HCO3-: 10       12    15     19    24     30    37

 Primary (Pure) Respiratory Disturbances:
   For each ∆ in pCO2 of 10, expect ∆ in pH of 0.08 in the
    opposite direction
   Example: (for a pure respiratory acidosis)
      If pCO2 = 70, then pH = 7.16
          Question #15
A 2-year-old girl with diarrheal dehydration secondary to
rotavirus gastroenteritis is admitted to the hospital.
Laboratory evaluation shows Na 132, K 4.2, Cl 104, HCO3
16, BUN 40, Cr 0.8, glucose 90, UpH 5.0, UNa 10, UK 10, UCl
40. Of the following, the MOST likely etiology of the
patient’s low HCO3 is:

 A.   Extrarenal losses of bicarbonate
 B.   Acute renal failure
 C.   Renal tubular acidosis, type IV
 D.   Munchausen by proxy
 E.   Lactic acidosis
Metabolic Acidosis
  Anion gap = Na+ – (Cl- + HCO3-)
        Normal anion gap: 8-14 mEq/L
Increased anion gap                       Normal anion gap
   “MUDPILES”                                 GI loss of HCO3-
      M=    Methanol, Metformin                 Diarrhea
      U=    Uremia                           Renal loss of HCO3-
      D=    DKA                                 Proximal (Type II) RTA
      P=    Paraldehyde                      Renal dysfunction
      I =   Inborn error of metabolism          Hyperkalemic (Type IV) RTA
      L =   Lactic acidosis
                                                 Distal (Type I) RTA
      E=    Ethylene glycol
                                              HCl, NH4Cl, arginine, lysine, or
      S=    Salicylates, Starvation
                                               carbonic anhydrase inhibitor
         Question #16
A 4-month-old former 27-week premie with chronic lung
disease presents with diarrhea and dehydration. Her
current medications include albuterol, furosemide, and
spironolactone. Laboratory evaluation reveals Na 132, K
2.9, Cl 84, HCO3 38, BUN 18, Cr 0.5, glucose 68. VBG
shows pH 7.56 and pCO2 52. What is the MOST likely
etiology of her metabolic alkalosis?
A. Diarrheal losses of HCO3
B. Compensatory response to primary respiratory
C. Dehydration
D. Furosemide side effect
E. Spironolactone side effect
Metabolic Alkalosis
 Loss of H+:
    GI losses: loss of gastric secretions (vomiting, pyloric
     stenosis, NG suctioning), antacid therapy
    Renal losses: loop or thiazide diuretics, mineralcorticoid
     excess, Conn syndrome, Cushing syndrome, Bartter
     syndrome, Gitelman syndrome, low chloride intake,
    H+ translocation into cells: hypokalemia, refeeding syndrome
 Retention of HCO3-:
    Massive blood transfusion (with citrated blood)
    Administration of NaHCO3
    Milk-alkali syndrome
 Contraction Alkalosis:
    Loop or thiazide diuretics
    GI losses (as above)
    Sweat chloride loss in cystic fibrosis
Metabolic Alkalosis
 Saline responsive (UCl < 25 mEq/L)
      Loss of gastric secretions (vomiting, gastric suctioning)
      Past diuretic use
      Cystic fibrosis
      Low chloride intake

 Saline non-responsive (UCl > 25-40 mEq/L)
    Mineralcorticoid excess (Conn and Cushing syndromes, black
     licorice ingestion, hyperreninemia)
    Severe hypokalemia
    Current diuretic usage
    Bartter and Gitelman syndromes
    Excess alkali administration
    Refeeding alkalosis
         Question #17
A 4-year-old presents to the emergency department with a
severe asthma exacerbation. Physical examination reveals
grunting, flaring, severe retractions, and diminished
aeration. Respiratory rate is 64 with oxygen saturation 86%
on 50% FIO2. Which of the following arterial blood gases is
MOST consistent with respiratory failure?

A.   pH 7.02, pCO2 24, and HCO3 6
B.   pH 7.70, pCO2 30, and HCO3 36
C.   pH 7.70, pCO2 50, and HCO3 60
D.   pH 7.02, pCO2 80, and HCO3 20
E.   pH 7.42, pCO2 38, and HCO3 24
Review Questions
 13 boards-style review questions with
  explanations in supplemental material
   Designed to test synthesis and application of
    the material presented

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