ACID-BASE

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					Fluids, Electrolytes &
Acid-Base Balance

                               Asiya Khanum
                     Lahore School of Nursing
Distribution of Body Fluids

    Total body water
        sum of all fluids within all compartments (60% of
         wgt)
  TBW expressed as % of body wgt in kgs
  1 liter weighs 2.2 lbs
  1milliliter = 1/1000 of a liter
  Rest of body weight
        Fat, bone etc
Distribution of Body Fluids

  Intracellular fluid (ICF) – within cells
  Extracellular fluid (ECF) - outside
        Interstitial fluid
             Space between cells and outside the blood vessels
        Intravascular fluid
             Blood plasma
        Other ECF compartments
             lymph, transcellular fluids (synovial, intestinal, CSF);
              sweat, urine, & peritoneal, pericardial, intraocular &
              pericardial fluids
Body Fluids: Movement of Fluids

    Diffusion
        Random movement of particles from higher concentration to
         area of lower concentration
    Osmosis
        Movement of water from lower to higher concentrations
         through a semi-permeable membrane
    Colloidal Osmotic Pressure
        Force to pull or absorb fluid from interstitial space
        Measurement of osmotic pressure
             Osmol: unit of osmotic pressure
             Osmolality: osmotic pull exerted by all particle per KG of water
             Osmolarity: osmotic pull per liter of solution
Water Movement Between ICF and ECF

  Primarily a function of osmotic forces
  Osmotic forces determined by sodium in ECF,
   potassium in ICF
Key Terminology

    Isotonic
        Same osmolality as intracellular fluids
             (280 mOsm/L)
             (iso-osmotic)
        Cells neither shrink nor swell – no change in RBC
         volume
        Net diffusion in and out of cell is zero
             Example: normal saline (0.9%), dextrose 5% in water
              (D5W)
Key Terminology

    Hypotonic
        Lesser osmolaltiy, or concentration than ICF (hypotonic to
         plasma)
        Water diffuses into the ICF, causing causing cells to swell
             Example: 0.45% sodium chloride
    Hypertonic
        Greater osmolality, than ICF
        Water rushes out of the cells to area of greater
         concentration, cells shrink, (water pulled out of cell)
             Example: 3% sodium chloride, 50% dextrose
Fluid Exchange at Capillary Level

    Capillary hydrostatic pressure
        Pressure pushing water out of the capillary into
         interstitial spaces
        Higher at arterial end (30-40 mmHg); lower at
         venous end (10-15 mmHg)
             Water moves out of the capillaries at arterial end, is
              reabsorbed at venous end
    Capillary colloidal osmotic pressure – osmotic
     pressure generated by plasma proteins
Factors Favoring Edema Formation

    Edema
        Accumulation of fluid within the interstitial spaces
         (form of “third spacing”)
  Increase capillary hydrostatic pressure
  Decrease capillary oncotic pressure
  Inflammation
        increase permeability
    Loss of lymphatic system
        obstruction
Clinical Manifestations-Edema

    Localized edema
        Site of trauma (ie finger)
        Organ system-cerebral or pulmonary
         edema, pleural/pericardial effusion, ascites
    Generalized edema
        Uniform distribution in interstitial spaces
    Dependent areas-feet, legs, sacral area,
     buttocks
        Pressure on tissues overlying bony prominences
             Pitting edema: pit left in skin
Clinical Manifestations-Edema

    Weight gain
    Swelling/puffiness
    Tight-fitting clothes
    Limited movement of affected area
    Sx assoc. w/underlying pathologic condition
    Slow wound healing
Edema – Assessment

    Visual inspection
    Determine degree of pitting w/finger pressure
    +1 (minimal) to +4 (severe)
    Measurement of abdominal circumference
    Daily weight
Edema - Tx

    Correct/control cause
    Prevent tissue injury
    Diuretic therapy
    Elevate feet
    Elastic support stockings
    Measure serum albumin
        Give IV albumin to raise colloidal osmotic pressure
         if low
Na+, Cl- & H20 Balance:
Water Balance
     Regulated by secretion of ADH & perception of
      thirst
     Thirst stimulates water drinking
     When water loss = 2% of body weight
     When increase in osmolality
     Osmoreceptors stimulated by dry mouth,
      hyperosmolality, plasma volume depletion;
      causes thirst
     Drinking water restores plasma volume, dilutes
      the ECF osmolality
ADH

    Release stimulated by:
        Plasma osmolality increases
        Circulating blood volume decreases
        Blood pressure drops
        Causes water to be reabsorbed into plasma from
         distal tubule of kidney
        Baroreceptors & volume receptors stimulate ADH
         release with dehydration from vomiting, diarrhea,
         excessive sweating
Water Balance

    Need 100 ml H20 per 100
     calories metabolized to dissolve and eliminate
     metabolic wastes
        Metabolic rate increases with fever
    Water gains
        Oral intake, oxidation of nutrients, GI tract
         absorption, cellular oxidation of fats, CHO
    Water losses
        Kidneys, lungs, skin, GI tract
Na+, Cl- and H20 Balance:
Sodium (Na+)

   Accounts for 90% of all cations (+)
   Most powerful ECF cation
   Primary regulator of water balance
         Regulates extracellular and vascular volume
          (essential for tissue perfusion)
   Maintains neuromuscular irritability for nerve
    conduction (w/K+, Ca+)
   Helps regulate acid base balance
         as base for sodium bicarbonate
Gains and Losses of Na+

    Sources of Na+
        Intake from dietary sources
        IV saline , medications
    Losses
        Mainly thru kidney
        Vomiting, diarrhea, fistula drainage, GI Suction
Sodium Balance

    Decreased circulating volume stimulates
     release of renin from kidney
    Release of renin converts angiotension to
     angiotension I
    Angiotension I converted to angiotension II
    Stimulates secretion of Aldoseterone 
     causes vasoconstriction
    Raises BP, restores renal perfusion
Sodium Balance

    Aldosterone promotes sodium and water
     reabsorption, increasing blood volume 
     further renin release in inhibited
Hyponatremia

  Serum Na+ < 135 mEq/L
  Serum osmolality < 280 mOsm/kg
  Artifactual / spurious: hyperlipidemia,
   hyperprotenemia
Hyponatremia

    Decrease Na+ w/ increase osmolality
        Excessive sweating (hot envir., w/exercise)
        GI losses – vomiting, diarrhea
        Diuresis
        Hyperglycemia
        hypoaldosteronism
    Decr. Na+ w/decrease osmolality
        D5W
        SIADH
        Impaired renal excretion
        Psychogenic polydipsia
Hyponatremia S & S

    Nervous system
         Headache
         Depression
         Personality changes
         Confusion
         Lethargy, weakness
         Stupor, coma
    GI
         Anorexia, nausea, vomiting
         Abdominal cramps
         Diarrhea
    Other – pitting edema
Hyponatremia Dx & Tx

  Dx: Lab values
  S & S, presence of predisposing conditions
  Tx: Focus on underlying cause
  Limit water intake, give IV hypertonic saline,
   loop diuretics, d/c meds that contribute to
   SIADH
Hypernatremia

    Na= > 148 mEq/l
    Serum osmolality > 295 mOsm/kg
    Excess water losses
        DI, diarrhea, watery diarrhea, hypertonic tube feedings
    Decreased water intake
        Oral trauma, inability to express thirst, impaired thirst
         sensation, withholding water(therapeutic), unconscious
    Excessive sodium intake
        Rapid/excessive admin. of IV saline, near-drowning in salt
         water
Hypernatremia S & S

  Increased thirst
  High urine specific gravity, oliguria or anuria
  Intracellular dehydration
        Dry, flushed skin, dry/sticky mucus membranes,
         rough/fissured tongue
        Decreased salivation/lacrimation
Hypernatremia S & S

    CNS
        Headache, agitation/restlessness, decreased
         reflexes, maniacal behavior, seizures, coma
    CV
        Tachycardia, decreased BP, weak/thready pulse
Hypernatremia Dx & Tx

    Lab values
    H&P
    Replacement of fluids, electrolytes
        Oral route preferred (oral glucose replacement for infants (IV if
         severe)
        WHO recommendations for oral rehydration
             Glucose preferred to sucrose (table sugar)
             contains specific amts of glucose, Na+, K+, CL-, bicarbonate
        No cola - contains no electrolytes, high sugar content may
         cause osmotic diarrhea
        Sport drinks – contain more Na and sugar
Chloride

    97-110 mE/L
    Major extracellular anion
    Provides electroneutrality
    Transport is passive, follows sodium
    Concentration varies inversely with changes
     ion bicarbonate (anion)
Disorders of Thirst & ADH Regulation

     Psychogenic Polydipsia
         Compulsive water drinking
         Drink large amts, excrete large amts of urine
         May be compounded by meds that increase ADH
          levels
         Leads to water intoxication
         Profound hyonatremia, hypo-osmolality
         Seizures, neurologic manifestations
         Tx: restrict water intake
Disorders of Thirst & ADH Regulation

     Syndrome of Inappropriate ADH (SIADH)
         Failure of negative feedback system that regulates
          release and inhibition of ADH
         ADH secretion continues despite decreases serum
          osmolality
         Marked retention of water in excess of sodium,
          dilutional hyponatremia
         Causes: lung/chest lesions, CNS disorders, drugs,
          pains, stress, temperature changes
         Tx: fluid restriction, diuretics, Lithium
Disorders of Thirst & ADH Regulation

     Diabetes Insipidus “Tasteless diabetes”
     Polyuria (excessive urination, dilute) & polydipsia due
      to disorder of ADH availability or function
     Triggered by increase in serum osmolality
     Central/neurogenic (defect in synthesis/release of
      ADH) or nephrogenic (kidneys do not respond to ADH)
     Excrete large volumes of urine (3-20 L/day); danger if
      unconscious, inadequate fluid intake
     Tx: Fix underlying problem; DDAVP
Potassium: K+

    2nd most abundant cation in body
    Major ICF cation
    All but about 2% of K+ is within body cells
        intracellular conc. 140-150 mEq/L
        Extracellular conc. 3.5-5.5 mEq/L
             what we measure on lab tests
    Gains
        from dietary sources (50-100 mEq/day if healthy; need more
         when stressed, trauma)
    Lost
        through kidney (80-90%); rest in stool, sweat
K+ Intracellular & Extracelluar Shifts

     Movement between ICF and ECF must be precise and
      efficient
     Transfer of even 1-2 % to ECF can dangerously
      elevate serum K+
     Movement into cell requires Na+/K+ pump
         Insulin increases movement of K+ into cells
         Acute increase if serum osmo moves K+ out of cells
         Acidosis – hydrogen ions moves into cell, K+ moves out
         Exercise – moves K+ of cell
K+ Regulation

    Eliminated by kidney – secreted into tubular
     fluid
        not reabsorbed
  Aldosterone also regulates secretion in
   collecting tubule
  Insulin
K+ Actions

    Critical to many cell functions
    Maintains intracellular osmolality
    Necessary for neuromuscular control
    Regulates skeletal, cardiac and smooth
     muscle activity
    Influences acid base balance
    Intracellular enzyme reactions
        CHO to energy; glucose to glycogen; conversion of
         amino acids to proteins
Hypokalemia < 3.5

    Causes
        Inadequate intake
             10-30 mEq/day compensates for obligatory urinary losses
             Elderly prone to deficit
        Excessive GI, renal, skin losses
             Increase urinary losses w/stress, trauma; diuretic therapy;
              burns, vomiting/diarrhea, fistula, GI suction
        Transcellular shifts
             Insulin, drugs (B-adrenergic agents like epi, albuterol)
Hypokalemia: Manifestations

  Gradual onset
  Kidney
        polyuria, nocturia  low urine osmo/spec grav
  Weakness and fatigue
  Weak respiratory muscles
  Nausea, vomiting, ileus
  Cardiac effects
        Flattened T wave
        Depressed ST segment
Hypokalemia TX

    Increase dietary intake
        Bananas, oranges, meats, dried fruits
    IV if need rapid replacement
        Need to fix magnesium deficiency first  impair K+
         correction
        Too rapid infusion can cause death
Hyperkalemia > 5.5

    Excess Intake/Gain
        Excess oral intake
        Excess/rapid infusion of replacement
        Tissue trauma, burns, crush injuries
    Inadequate renal losses
        Renal failure
        Adrenal insufficiency (Addison’s)
        RX with K+ sparing diuretics and ACE inhibitors
Manifestations Hyperkalemia

    Muscular weakness, paresthesia, paralysis
    Nausea, diarrhea
    Oliguria
    Cardiac effects
    Tall, tented T wave; depressed T segments;
     widened QRS, cardiac arrest
Tx Hyperkalemia

  Varies with severity of disturbance
  Restrict dietary sources
  Dialysis if renal failure
  Enema with exchange resins
Calcium, Phosphate, Magnesium

    Need for many metabolic functions
        Ingested in diet, absorbed form intestine, filtered in
         kidney (glomerulus), reabsorbed in renal tubules,
         eliminated in urine
        Most found in bone, small amt in cells, sm amt in
         ECF
    ECF concentration is vital
        Regulated by parathyroid hormone (PTH) and
         vitamin D
        Reciprocal regulation: Ca high, phos low
Vitamin D & PTH

    Vit D
        Role: Increase plasma levels of Calcium and phos;
         maintain favorable condition for bone mineralization
        Increases intestinal absorption of calcium and
         phosphorous
    PTH
        Maintains normal ECF concentration of calcium
        Synthesized in parathyroid glands
Calcium

    Normal serum concentration 8.5-10.5 mg/dl (ionized
     4.5-5.6)
    Gains: dietary
    Total serum Ca+ changes w/alterations in albumin &
     pH
        decr w/ decr albumin and rise in pH (bound to plasma protein)
    50% of serum Ca= is ionized: can leave the vascular
     compartment & participate in cellular functions
    Cell membrane potential, contaction of skeletal and
     cardiac muscle
Hypocalcemia < 8.5 mg/dl

    Causes
        Surgical hypoparathyroidism
        Acute pancreatitis (seqestration of Ca+)
        Other electrolytes abn (hypomagnesemia,
         hyperphosphatemia)
        Malabsorption problems
        Infusion of citrate in blood
        Drugs (phenytoin)
        Vit D deficiency
Hypocalcemia Manifestations

    Neuro
        Decreased ionized calcium
        Paresthesias (espec. numbness, tingling)
        Skeletal/abd muscle cramps
        Carpopedal spasms
        Tetany
        Laryngeal spasm
        Pos Chvostek’s and Trousseau’s signs
Hypocalcemia Manifestations

    CV
        Hypotension
        Cardiac insufficiency
    Bone – Chronic calcium deficit
        Osteomalacia
        Bone pain, deformities, fractures
Hypocalcemia: Tx

  Acute hypocalcemia is emergency
  Chronic – oral intake
        One glass of milk = 300 mg
        supplements
Hypercalcemia > 10.5 mg/dl

    Causes
        Neoplasms/malignancies
        Primary hyperparathyroidism
        Prolonged immobolization
        Drugs (lithium, thiazide diuretics, excessive use of
         Ca+ during cardiac arrest)
Hypercalcemia Manifestations

    Neuromuscular
         Muscle weakness, atrophy
         Ataxia, loss of muscle tone
    GI
         Anorexia, N & V, constipation
    Behavior/CNS
         Lethargy, personality and behavior changes, stupor/coma
    Renal
         Polyuria, flank pain, renal insufficiency, kidneys stones
    CV
         Hypertension, short QT interval, AV block
Hypercalcemia Tx

    Recognize high risk pts
    Re-hydration
    0.9 % NaCl
    Increase urinary excretion
    Loop diuretics
    Inhibit bone reabsorption
    Drugs to inhibit mobilization (plicamycin,
     calcitonin)
Magnesium

  Normal: 1.8 – 2.7 mg/dl (1.5 – 2.5)
  Sources
  Dietary
        eliminatd thru kidneys, GI system
    Can be given IV
        33% bound to protein or ionized
    Stored in muscle and bone
Magnesium

    Functions
    Needed for intracellular enzymatic reactions
    Neuromuscular excitability
    Cardiac and skeletal muscle contraction
    Smooth muscle relaxation
Hypomagnesemia

  Less than 1.5mg/dl
  GI losses
        malabsorption, malnutition, laxative abuse
  Chronic alcoholism
  Usually ocurs with hypocalcemia, hypokalemia
Hypomagnesemia

    Manifestations
        Neuromuscular
             irritability, tremors, personality changes, nystagmus,
              seizures
        CV
             tachycardia, hypertension, dysrhyrhmias
        TX
             Prevent/early detection
             IV repletion
Hypermagnesemia

  >2.7 mg/dl (2.1)
  Causes
        Excessive intake, inadequate excretion (renal
         insufficiency)
        Manifestations
             Neuromuscular
                  hyporeflexia, muscle weakness, confusion, coma
             Resp
                  muscle paralysis
             CV
                  hypotension, incr. PR interval, short QT interval, cardiac
                   arrest
Dehydration

    3 Major Types
        Isotonic - Fluid has the same osmolarity as plasma
        Hypotonic -Fluid has fewer solutes than plasma
        Hypertonic-Fluid has more solutes than plasma
Isotonic Dehydration

    Most common form of dehydration
        fluids and electrolytes are lost in even amounts
        no intercellular fluid shifts
    Common Causes
        diuretic therapy
        excessive vomiting
        excessive urine loss
        hemorrhage
        decreased fluid intake
Assessment of Isotonic Dehydration

    Weight Loss
    Hypotension and Orthostatic Hypotension
    Rapid, weak pulse
    Oliguria - (dark, concentrated, scanty urine)
    Decreased skin turgor
    Dry mucous membranes
    Elevated urine specific gravity
    Altered Level of Consciousness
    Increased Hematocrit (except in hemorrhage), serum
     protein and BUN
    Severe Isotonic Dehydration can lead to SHOCK
Interventions for Isotonic Dehydration

     Monitor daily weight, I&O, Skin turgor, LOC
      and V.S.
     Check Skin turgor on forehead or sternum on
      elderly
     Monitor Lab values - Urine SpG, BUN, CBC
      and electroytes
     Replace fluid loss using ISOTONIC fluids
     Treat the underlying cause
Hypertonic Dehydration

    Second most common type of dehydration
        water loss from ECF is greater than solute loss
    Prevention of Hypertonic dehydration
        Prevent Insensible Fluid Loss - Hyperventilation, pure water
         loss with high fevers, and watery diarrhea.
        Control Disease Processes - Diabetic Ketoacidosis and
         Diabetes Insipidus
        Prevent Iatrogenic Causes - Prolonged NPO, excessive
         administration of hypertonic fluids, sodium bicarbonate, or
         tube feedings with inadequate amounts of water
Assessment of Hypertonic Dehydration

    Causes fluid to be pulled from the cells into the blood
     stream
        leading to cellular shrinkage
    Thirst
    Decreased Skin Turgor
    Dry Mucous Membranes
    Increased Serum Sodium and Serum Osmolarity
    Increased Urine Specific Gravity
    Signs of Shock are usually not present
Interventions for Hypertonic Dehydration

     Prevent Hypertonic Dehydration
         Dilute tube feedings with adequate amounts of
          water
         Monitor I&O, daily weight, skin turgor, LOC, Serum
          Sodium and Serum Osmolarity
         Administer Hypotonic fluids orally or SLOWLY by IV

         Be aware that rapid administration of hypotonic IV
          fluids can cause swelling of the brain cells, and
          increased intercrainal pressure
Hypotonic Dehydration

    Relatively Uncommon
        Loss of more solute (usually sodium) than water
    Causes fluid to shift from the blood stream into the
     cells
        leading to decreased vascular volume and eventual shock
    Seen in Heat Exhaustion
    Increased cellular swelling  causes increased
     intercranial pressure  H/A and Confusion
    Seen in Heat Stroke
Prevention of Hypotonic Dehydration

     Avoid over administration of hypotonic fluids –
         Most common cause of hypotonic dehydration
     Replace fluid loss during exercise with isotonic fluids
      to patients with Isotonic dehydration
     Select the correct IV fluid and rate to meet patients
      rehydration needs
     Watch for low serum osmolarity and serum sodium
     Persons at Risk
         Persons with Chronic Renal Failure, Persons with Chronic
          Malnutrition
Assessment of Hypotonic Dehydration

    Hypotension
    Tachycardia
    Changes in LOC
    Low Serum Sodium
    Low Serum Osmolarity
    Low Urine Specific Gravity
    Increased Urine Volume
Interventions for Hypotonic Dehydration

   Treat the underlying cause
   Rehydrate orally with hypertonic fluids
   IV administration of NS to restore sodium
    balance
   In rare instances hypertonic Sodium (NS 3%)
    may be used
SHOCK

  Shock is the body's reaction to decreased
   tissue perfusion
  Common causes
        Acute fluid loss - Hypovolemic Shock
        Heart Failure - Cardiogenic Shock
        Neurogenic Shock - results in dilation of blood
         vessels
        Vasogenic Shock - due to acute allergic reactions
        Septic Shock - due to the release of bacterial
         endotoxcins
SHOCK
Assessment of Shock

    Hypotension
    Cold, moist, clammy skin
    Deep, rapid respirations
    Decreased urinary output
    Thirst
    Changes in LOC
    Early - Apprehension and restlessness
    Late - Lethargy to coma
Interventions for Shock

    Goal is to increase ECF volume and pressure
        To increase tissue perfusion
    Maintain airway
    Start O2 if indicated
    Position with legs elevated 45 degrees
    Keep warm
    Start IV
        Start N/S, be ready to give blood or plasma expanders if
         indicated
    Cardiac Monitor
    MAST or other external pressure devices can be used
     for hypovolemic shock
Acid Base Balance

  pH of ECF maintained at very narrow range:
   7.35-7.45
  Acid
        Can release hydrogen ion
        Dissociates reversibly when added to water to form
         H+ and anions
        Degree of dissociations depends on if strong or
         weak acid (same true of base)
    Base
        Can accept hydrogen ion
pH

  H+ ion expressed in terms of pH
  pH = the negative logarithm (p) of the H+ ion
   concentration in equivalents per liter
        pH of 7.0 implies a H+ ion concentration of 10-7
         equivalents per liter (mEq/L)
    pH inversely related to H+ ion concentration
        Low pH = high concentration of H+ ions
        High pH = low concentration of H+ ions
CO2 and NaHCo3

    Body metabolism results in CO2 production
        CO2 transported in 3 forms
             Attached to hemoglobin
             As dissolved CO2
             As bicarbonate
    Co2 not an acid
        small % of gas combines w/water in bloodstream to
         form carbonic acid
    Rxn b/t CO32 and H2O is catalyzed by
     carbonic anhydrase
        present ion RBC’s, renal tubular cells, body tissue
pH

  Henderson-Hasselbalch equation
  Ratio rather than absolute values for bicarb
   and dissolved CO2 that determines pH
        pH remains relatively stable over a wide range of
         changes in bicarb/CO2
             providing the 2 approach concentration of 20:1
        pH decreases when ratio is less than 20 to 1
        pH increases when ration is greater than 20 to 1
pH

  Bicarb part of HH equation controlled by
   generation of metabolic acids and avail of
   bicarb to buffer
  H2CO3 regulated by respiration
  Kidney generates and recycles bicarb and
   contributes to metabolic part of equation
Buffer systems

    Proteins
        acid or base
    Bicarbonate buffer system
        Carbonic acid, bicarbonate
  Plasma Potassium-Hydrogen Exchange
  Respiratory control mechanisms
  Renal control mechanisms
Respiratory Control Mechanisms

  Elimination of CO2
  H+ ion stimulates respiratory center
        increase or decrease in ventilation
    Respiratory control of pH is rapid
        occurs within minutes, max at 12-4 hrs
    Does not completely return pH to normal
Renal Control Mechanisms

  Happens slower than respiratory - hrs to days
  Eliminate H= ion
        conserve base
Laboratory Tests

    Arterial blood gases (ABG’s)
        pH
        CO2 content
        Bicarbonate
        Base excess/deficit
        Anion gap
Acid-Base Disorders

    Metabolic
        Alteration in bicarbonate
        Result from addition or loss of acid or alkali from
         ECF
        Metabolic acidosis
             Decrease pH due to reduced bicarbonate
        Metabolic alkalosis
             Elevated pH due to increased bicarbonate
Acid-Base Disorders

    Respiratory
        Disorder in PCO2 (increase or decrease in alveolar
         ventilation)
        Respiratory Acidosis
             Decrease pH, increased PCO2
             Decreased alveolar ventilation
        Respiratory Alkalosis
             Increased pH, increased alveolar ventilation, decreased
              PCO2
Metabolic Acidosis

    Acids increase or bicarbonate is lost
    Can occur quickly (lactic acidosis) or over time (renal
     failure, diabetic ketoacidosis)
    If severe, buffering systems cannot compensate
    Early sx: headache, lethergy; progress to coma if
     severe acidosis
    Resp compensation: Kussmaul respirations
        deep, rapid-try to blow off CO2
    Other: anorexia, N&V, diarrhea, abd discomfort, death
Metabolic Alkalosis

    Excessive loss of metabolic acid, bicarb increases
    If acid lost by vomiting, renal comp. Not very effective
     (loss of CL- in HCL stimulates renal retention of
     bicarb)
    Diuretics –may prodcue mild alkalosis (promote more
     excretion of Na+, K=. CL- than bicarb)
    Weakness, muscle cramps, hyperactive reflexes,
     tetany, shallow slow resp., confusions, sz
Respiratory Acidosis

    Decrease in alveolar ventilation in relation to
     CO2 production, increased carbonic acid
        acidosis
    Occurs with depression of ventilation
        increased CO2 (hypercapnia)
Respiratory Acidosis

  Depression of respiratory center
  Respiratory muscle paralysis
  Disorders of chest wall (kyphoscolosis,
   pickwickian syndrome, flail chest/trauma)
  Disorders of lung parenchyma (pneumonia,
   pulm edema, asthma, emphysema)
Respiratory Acidosis

  Can be acute or chronic
  Renal compensation
        occurs by elimination of H+ and retention of CO2
  Restlessness, apprehension followed by
   lethargy, tremors, coma
  Respiratory rate rapid initially, then becomes
   depressed
        respiratory center adapts to rising CO2
Respiratory Alkalosis

    Alveolar hyperventilation
        hypocapnia
    Hypermetabolic states (stimulate hyperventilation)
        fever, anemia, high altitudes
        early salicylate intoxication, hysteria, cirrhosis, gm- sepsis
         Improper use of mechanical ventilation
    Kidneys compesate
        By decreasing H+ excretion or HCO3-reabsorption
    Dizziness, confusion, tingling of extremities
     (paresthesias), sz, coma, deep rapid respirations
The End