iv therapy - presentation

8/6/2019 IV Therapy - Presentation

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FLUID Therapy

Dan Belz, July 2008


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F luid and electrolyte balance is anextremely complicated thing.


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I mportance

Need to make a decision regarding fluids in prettymuch every hospitalized patient.

Can be life-saving in certain conditionsloss of body water, whether acute or chronic, cancause a range of problems from mildlightheadedness to convulsions, coma, and in

some cases, death.Though fluid therapy can be a lifesaver, it's never innocuous, and can be very harmful.


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K inds of IV F luid solutions

Hypotonic - 1/2NSI sotonic - NS, LR, albumenHypertonic Hypertonic saline.

CrystalloidColloid


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Crystalloid vs ColloidType of particles (large or small)

F luids with small crystalizable particles like NaCl are called crystalloids

F luids with large particles like albumin are calledcolloids , these dont (quickly) fit through vascular

pores, so they stay in the circulation and muchsmaller amounts can be used for same volume

expansion. (250ml Albumin = 4 L NS) Edema resulting from these also tends to stick aroundlonger for same reason.

Albumin can also trigger anaphylaxis.


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There are two components to fluid therapy:M aintenance therapy replaces normalongoing losses, andR eplacement therapy corrects any existingwater and electrolyte deficits.


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M aintenance therapy

M aintenance therapy is usually undertaken whenthe individual is not expected to eat or drink normally for a longer time (eg, perioperatively or on a ventilator).Big picture: M ost people are NPO for 12 hourseach day.

Patients who wont eat for one to two weeksshould be considered for parenteral or enteralnutrition.


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M aintenance Requirements can be brokeninto water and electrolyte requirements:


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W ater

Two liters of water per day are generally sufficient for adults;M ost of this minimum intake is usually derived from thewater contentof food and the water of oxidation, thereforeit has been estimated that only 500ml of water needs beimbibed 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 bymaintenance fluids.


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water requirements increase with:fever, sweating, burns, tachypnea, surgical

drains, polyuria, or ongoing significantgastrointestinal losses.

F or example, water requirements increase by 100to 150 mL/day for each C degree of bodytemperature elevation.


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Several formulas can be used to calculate maintenance fluid rates.


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A comparison of formulas produces a widevariety of fluid recommendations:

2000 cc to 3378 cc for an obese woman who is65 inches tall and weighs 248 pounds (112.6 kg)This is a reminder that fluid needs, no matter whatformula is used, are at best an estimation.


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4/2/1 rule4 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 kgthen you add 1 ml/kg/hr for each kg over 20 kg

This boils down to:W

eight in kg + 40 =M

aintenanceIV

rate/hour.F or any person weighing more than 20kg


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M aintenance IV rate:4/2/1 rule -> W eight in kg + 40


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W hat to put in the fluids


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Start: D5 1/2NS+20 meq K @ W t+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 @ W t+40/hr)

Glucose in the form of dextrose (D5) can be added to provide some calorieswhile the patient is NPO.

The normal kidney can maintain sodium and potassium balance over a widerange 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.


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Start D5 1/2NS+20 meq K , then adjust:

I f sodium falls, increase the concentration(eg, to NS)I f sodium rises, decrease the concentration(eg, 1/4NS)I f the plasma potassium starts to fall, add

more potassium.I f things are good, leave things alone.


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U sually kidneys regulate well, but:Altered homeostasis in the hospital

I n the hospital, stress, pain, surgery canalter the normal mechanisms.I ncreased aldosterone, I ncreased ADHThey generally make patients retain morewater and salt, increase tendency for edema, and become hypokalemic.


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Now onto Part 2 of the presentation:


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Hypovolemia

H ypovolemia or FVD is result of water &electrolyte loss

Compensatory mechanisms include:I ncreased sympathetic nervous systemstimulation with an increase in heart rate& cardiac contraction; thirst; plusrelease of AD H & aldosteroneSevere case may result in hypovolemicshock or prolonged case may cause renalfailure


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Causes of FV D=hypovolemia:

Gastrointestinal losses: N/ V /DRenal losses: diureticsSkin or respiratory losses: burns

Third-spacing: intestinal obstruction, pancreatitis


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R eplacement therapy.


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A variety of disorders lead to fluid lossesthat deplete the extracellular fluid .This can lead to a potentially fatal decreasein tissue perfusion.F ortunately, early diagnosis and treatmentcan restore normovolemia in almost allcases.


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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 bloodflow.This needs rapid treatment with isotonic fluid boluses (1-2L NS), and assessment and treatment of the underlyingcause.But hypovolemia that is less severe and therefore wellcompensated is more difficult to accurately assess.


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History for assessing hypovolemia

The history can help to determine the presence and etiology of volumedepletion.W eight loss!Early complaints include lassitude, easy fatiguability, thirst, muscle cramps,

and postural dizziness.M ore severe fluid loss can lead to abdominal pain, chest pain, or lethargy andconfusion due to ischemia of the mesenteric, coronary, or cerebral vascular

beds, respectively. Nausea and malaise are the earliest findings of hyponatremia, and may beseen when the plasma sodium concentration falls below 125 to 130 meq/L.This may be followed by headache, lethargy, and obtundation

M uscle weakness due to hypokalemia or hyperkalemiaPolyuria and polydipsia due to hyperglycemia or severe hypokalemiaLethargy, confusion, seizures, and coma due to hyponatremia, hypernatremia,or hyperglycemia


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Basic signs of hypovolemia

U rine output, less than 30ml/hr Decreased BP, I ncrease pulse


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Physical exam for assessing volume

physical exam in general is not sensitive or specificacute weight loss; however, obtaining an accurate weight over time may bedifficultdecreased skin turgor - if you pinch it it stays put

dry skin, particularly axilladry mucus membraneslow arterial blood pressure (or relative to patient's usual BP)orthostatic hypotension can occur with significant hypovolemia; but it is alsocommon in euvolemic elderly subjects.decreased intensity of both the K orotkoff sounds (when the blood pressure is

being measured with a sphygmomanometer) and the radial pulse ("thready")due to peripheral vasoconstriction.decreased Jugular V enous PressureThe normal venous pressure is 1 to 8 cmH2O, thus, a low value alone may benormal and does not establish the diagnosis of hypovolemia.


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SI GNS & SY M PTO M S O F F luidV olume Excess

SOB & orthopneaEdema & weight gainDistended neck veins & tachycardia

Increased blood pressure

Crackles & wheezespleural effusion


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F or the EB M aficionados out there.

A JA M A 1999 systematic review of physical diagnosis of hypovolemia in adultsCONCL U SI ONS: A large postural pulse change (> or =30

beats/min) or severe postural dizziness is required toclinically diagnose hypovolemia due to blood loss,although these findings are often absent after moderateamounts of blood loss. I n 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 diagnosticcertainty is required.


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W hich brings us to:Labnormalities seen with hypovolemia

a variety of changes in urine and bloodoften accompany extracellular volumedepletion.I n addition to confirming the presence of volume depletion, these changes may

provide important clues to the etiology.


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BU N/Cr

BU N/Cr ratio normally around 10I ncrease above 20 suggestive of prerenal state

(rise in B U N without rise in Cr called prerenalazotemia.)This happens because with a low pressure head

proximal to kidney, because urea (B U N) isresorbed somewhat, and creatinine is secretedsomewhat as well


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Hgb/Hct

Acute loss of EC fluid volume causeshemoconcentration (if not due to bloodloss)Acute gain of fluid will cause hemodilutionof about 1g of hemoglobin (this happens

very often.)


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Plasma Na

Decrease in I ntravascular volume leads togreater avidity for Na (through aldosterone)AND water (through ADH),So overall, Plasma Na concentration tendsto decrease from 140 when hypovolemia

present.


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U rine Na

U rine Na goes down in prerenal states as body tries to hold onto water.Getting a F ENa helps correct for urineconcentration.Screwed up by lasix.Calculator on PDA or medcalc.com


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IV M odes of administration

Peripheral IV

PI CCCentral LineI ntraosseous


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IV Problem:Extravasation / I nfiltrated

The most sensitive indicator of extravasatedfluid or "infiltration" is to transilluminatethe skin with a small penlight and look for the enhanced halo of light diffusion in thefluid filled area.

Checking flow of infusion does not tell youwhere the fluid is going


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Thats it folks.

iv therapy - presentation

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