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Fluid and electrolyte balance is an
extremely complicated thing.

Importance
 Need to make a decision regarding fluids in pretty
much every hospitalized patient.
 Can be life-saving in certain conditions
 loss of body water, whether acute or chronic, can
cause a range of problems from mild
lightheadedness to convulsions, coma, and in
some cases, death.
 Though fluid therapy can be a lifesaver, it's never
innocuous, and can be very harmful.

Kinds of IV Fluid solutions
 Hypotonic - 1/2NS
 Isotonic - NS, LR, albumen
 Hypertonic – Hypertonic saline.
 Crystalloid
 Colloid

Crystalloid vs Colloid
Type of particles (large or small)
 Fluids with small “crystalizable” particles like
NaCl are called crystalloids
 Fluids with large particles like albumin are called
colloids, these don’t (quickly) fit through vascular
pores, so they stay in the circulation and much
smaller amounts can be used for same volume
expansion. (250ml Albumin = 4 L NS)
– Edema resulting from these also tends to stick around
longer for same reason.
– Albumin can also trigger anaphylaxis.

There are two components to fluid therapy:
 Maintenance therapy replaces normal
ongoing losses, and
 Replacement therapy corrects any existing
water and electrolyte deficits.

Maintenance therapy
 Maintenance therapy is usually undertaken when
the individual is not expected to eat or drink
normally for a longer time (eg, perioperatively or
on a ventilator).
 Big picture: Most people are “NPO” for 12 hours
each day.
 Patients who won’t eat for one to two weeks
should be considered for parenteral or enteral
nutrition.

Maintenance Requirements can be broken
into water and electrolyte requirements:

Water —
 Two liters of water per day are generally sufficient for
adults;
 Most of this minimum intake is usually derived from the
water content
of food and the water of oxidation, therefore
 it has been estimated that only 500ml of water needs be
imbibed given normal diet and no increased losses.
 These sources of water are markedly reduced in patients
who are not eating and so must be replaced by
maintenance fluids.

 water requirements increase with:
fever, sweating, burns, tachypnea, surgical
drains, polyuria, or ongoing significant
gastrointestinal losses.
 For example, water requirements increase by 100
to 150 mL/day for each C degree of body
temperature elevation.

Several formulas can be used to calculate maintenance fluid rates.

 A comparison of formulas produces a wide
variety of fluid recommendations:
 2000 cc to 3378 cc for an obese woman who is
65 inches tall and weighs 248 pounds (112.6 kg)
 This is a reminder that fluid needs, no matter what
formula is used, are at best an estimation.

4/2/1 rule a.k.a Weight+40
 I prefer the 4/2/1 rule (with a 120 mL/h
limit) because it is the same as for
pediatrics.

 4/2/1 rule
4 ml/kg/hr for first 10 kg (=40ml/hr)
then 2 ml/kg/hr for next 10 kg (=20ml/hr)
then 1 ml/kg/hr for any kgs over that
This always gives 60ml/hr for first 20 kg
then you add 1 ml/kg/hr for each kg over 20 kg
This boils down to: Weight in kg + 40 = Maintenance IV rate/hour.
For any person weighing more than 20kg

Maintenance IV rate:
4/2/1 rule -> Weight in kg + 40

Start: D5 1/2NS+20 meq K @ Wt+40/hr
 a reasonable approach is to start 1/2 normal saline to which 20 meq of
potassium chloride is added per liter.
(1/2NS+20 K @ Wt+40/hr)
 Glucose in the form of dextrose (D5) can be added to provide some calories
while the patient is NPO.
 The normal kidney can maintain sodium and potassium balance over a wide
range of intakes.
 So,start:
D5 1/2NS+20 meq K
at a rate equal to their weight + 40ml/hr, but no greater than 120ml/hr.
 then adjust as needed, see next page.

Start D5 1/2NS+20 meq K, then adjust:
 If sodium falls, increase the concentration
(eg, to NS)
 If sodium rises, decrease the concentration
(eg, 1/4NS)
 If the plasma potassium starts to fall, add
more potassium.
 If things are good, leave things alone.

Usually kidneys regulate well, but:
Altered homeostasis in the hospital
 In the hospital, stress, pain, surgery can
alter the normal mechanisms.
 Increased aldosterone, Increased ADH
 They generally make patients retain more
water and salt, increase tendency for
edema, and become hypokalemic.

Now onto Part 2 of the presentation:

Hypovolemia
 Hypovolemia or FVD is result of water &
electrolyte loss
 Compensatory mechanisms include:
Increased sympathetic nervous system
stimulation with an increase in heart rate
& cardiac contraction; thirst; plus
release of ADH & aldosterone
 Severe case may result in hypovolemic
shock or prolonged case may cause renal
failure

Causes of FVD=hypovolemia:
 Gastrointestinal losses: N/V/D
 Renal losses: diuretics
 Skin or respiratory losses: burns
 Third-spacing: intestinal obstruction,
pancreatitis

 A variety of disorders lead to fluid losses
that deplete the extracellular fluid .
 This can lead to a potentially fatal decrease
in tissue perfusion.
 Fortunately, early diagnosis and treatment
can restore normovolemia in almost all
cases.

 There is no easy formula for assessing the degree of
hypovolemia.
 Hypovolemic Shock, the most severe form of hypolemia,
is characterized by tachycardia, cold, clammy extremities,
cyanosis, a low urine output (usually less than 15 mL/h),
and agitation and confusion due to reduced cerebral blood
flow.
 This needs rapid treatment with isotonic fluid boluses (1-
2L NS), and assessment and treatment of the underlying
cause.
 But hypovolemia that is less severe and therefore well
compensated is more difficult to accurately assess.

History for assessing hypovolemia
 The history can help to determine the presence and etiology of volume
depletion.
 Weight loss!
 Early complaints include lassitude, easy fatiguability, thirst, muscle cramps,
and postural dizziness.
 More severe fluid loss can lead to abdominal pain, chest pain, or lethargy and
confusion due to ischemia of the mesenteric, coronary, or cerebral vascular
beds, respectively.
 Nausea and malaise are the earliest findings of hyponatremia, and may be
seen when the plasma sodium concentration falls below 125 to 130 meq/L.
This may be followed by headache, lethargy, and obtundation
 Muscle weakness due to hypokalemia or hyperkalemia
 Polyuria and polydipsia due to hyperglycemia or severe hypokalemia
 Lethargy, confusion, seizures, and coma due to hyponatremia, hypernatremia,
or hyperglycemia

Basic signs of hypovolemia
 Urine output, less than 30ml/hr
 Decreased BP, Increase pulse

Physical exam for assessing volume
 physical exam in general is not sensitive or specific
 acute weight loss; however, obtaining an accurate weight over time may be
difficult
 decreased skin turgor - if you pinch it it stays put
 dry skin, particularly axilla
 dry mucus membranes
 low arterial blood pressure (or relative to patient's usual BP)
 orthostatic hypotension can occur with significant hypovolemia; but it is also
common in euvolemic elderly subjects.
 decreased intensity of both the Korotkoff sounds (when the blood pressure is
being measured with a sphygmomanometer) and the radial pulse ("thready")
due to peripheral vasoconstriction.
 decreased Jugular Venous Pressure
 The normal venous pressure is 1 to 8 cmH2O, thus, a low value alone may be
normal and does not establish the diagnosis of hypovolemia.

SIGNS & SYMPTOMS OF Fluid
Volume Excess
 SOB & orthopnea
 Edema & weight gain
 Distended neck veins & tachycardia
 Increased blood pressure
 Crackles & wheezes
 pleural effusion

For the EBM aficionados out there.
 A JAMA 1999 systematic review of physical diagnosis of
hypovolemia in adults
 CONCLUSIONS: A large postural pulse change (> or =30
beats/min) or severe postural dizziness is required to
clinically diagnose hypovolemia due to blood loss,
although these findings are often absent after moderate
amounts of blood loss. In patients with vomiting, diarrhea,
or decreased oral intake, few findings have proven utility,
and clinicians should measure serum electrolytes, serum
blood urea nitrogen, and creatinine levels when diagnostic
certainty is required.

Which brings us to:
Labnormalities seen with hypovolemia
 a variety of changes in urine and blood
often accompany extracellular volume
depletion.
 In addition to confirming the presence of
volume depletion, these changes may
provide important clues to the etiology.

BUN/Cr
 BUN/Cr ratio normally around 10
 Increase above 20 suggestive of “prerenal state”
 (rise in BUN without rise in Cr called “prerenal
azotemia.”)
 This happens because with a low pressure head
proximal to kidney, because urea (BUN) is
resorbed somewhat, and creatinine is secreted
somewhat as well

Hgb/Hct
 Acute loss of EC fluid volume causes
hemoconcentration (if not due to blood
loss)
 Acute gain of fluid will cause hemodilution
of about 1g of hemoglobin (this happens
very often.)

Plasma Na
 Decrease in Intravascular volume leads to
greater avidity for Na (through aldosterone)
AND water (through ADH),
 So overall, Plasma Na concentration tends
to decrease from 140 when hypovolemia
present.

Urine Na
 Urine Na – goes down in prerenal states as
body tries to hold onto water.
 Getting a FENa helps correct for urine
concentration.
 Screwed up by lasix.
 Calculator on PDA or medcalc.com

IV Modes of administration
 Peripheral IV
 PICC
 Central Line
 Intraosseous

IV Problem:
Extravasation / “Infiltrated”
 The most sensitive indicator of extravasated
fluid or "infiltration" is to transilluminate
the skin with a small penlight and look for
the enhanced halo of light diffusion in the
fluid filled area.
 Checking flow of infusion does not tell you
where the fluid is going

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045_6_fluids_advanced.ppt

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