Fluid Therapy,Acid-Base and Electrolyte Imbalance(Dr.tini)

8/10/2019 Fluid Therapy,Acid-Base and Electrolyte Imbalance(Dr.tini)

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Fluid Therapy , Acid-Base and

Electrolyte Imbalance

Perioperative & Acute Care Surgery Course


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Henderson-Hasselbalch Stewarts Approach

Measuring acid-basedisorders


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HOW TO UNDERSTAND ACID-BASE

A quanti tat ive Ac id-Base Primer

For Bio logy and Medic inePeter A. Stewart

Edward Arno ld, London 1981

Stewart PA, 1981


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DUA VARIABEL

pH atau [H+] DALAM PLASMADITENTUKAN OLEH

VARIABELINDEPENDEN

VARIABELDEPENDEN

Menurut Stewart ;

Menentukan

Stewart PA. Can J Physiol Pharmacol 61:1444-1461, 1983.

Primer (cause) Sekunder (effect)


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VARIABEL INDEPENDEN

CO2 STRONG IONDIFFERENCE WEAK ACID

pCO2SID Atot

Diatur olehsistim respirasi

Ditentukan olehkomposisi

elektrolit darah(diatur oleh ginjal)

Ditentukan olehkonsentrasi protein(diatur oleh hati dankeadaan metabolik)


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DEPENDENT VARIABLES

H

+

OH-

CO3= A-

AH

HCO3-


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Gamblegram

Na+

K+ 4Ca++Mg++

Cl

-

HCO3-

KATION ANION

SID

STRONG ION DIFFERENCE

= {[Na+] + [K+] + [kation divalen]} - {[Cl-] + [As.organik kuat-]}

As. Organik kuat

Weak acid(Alb-,P-)

SID


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ClNa

Hubungan SID, H+& OH-

SID() (+)

[H+] [OH-]

Dalam cairan biologis (plasma) dgn suhu 370C, SID selalu positif,nilainya berkisar 30-40 mEq/Liter

Asidosis Alkalosis

Konsentrasi H+

Na

S

ClNa

Cl

S

SID


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Na140

K

MgCa

Cl

102

PO4

Alb

SID = 34

Cl

115

Alb

PO4

SID

Asidosishiperklor

Cl

102

Laktat/keto

AsidosisKeto/laktat

CL 95

Alb

PO4

Alkalosishipoklor

SID

SID

Perubahan pada SID dan Weak Acid

PO4

Alb

Normal

Cl

102

SID

Alkalosishipoalb/fosfat

Cl

102

SID

Alb/PO4

Asidosishiperalb/

fosfat


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Sebagian besar cairan kristalloid & koloid yang ada

mengandung campuran elektrolit yang tidak fisiologis

un-balanced

Pada awal 1990, mulai dikenal dan didefinisikan

hyperchloremic acidosis

,pasca infusi cairan NaCl .

Penggunaan dalam jumlah besar dari cairan un-balanced ini

dapat berakibat gangguan keseimbangan asam-basa


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Respirasi Hiperventilasi

Penurunan kekuatan otot nafasdan menyebabkan kelelahan otot

Sesak

Metabolik Peningkatan kebutuhan

metabolisme

Resistensi insulin

Menghambat glikolisis anaerob

Penurunan sintesis ATP

Hiperkalemia Peningkatan degradasi protein

Otak Penghambatan metabolisme dan

regulasi volume sel otak

Koma

Kardiovaskular Gangguan kontraksi otot jantung

Dilatasi arteri,konstriksi vena, dansentralisasi volume darah

Peningkatan tahanan vaskular paru

Penurunan curah jantung, tekanandarah arteri, dan aliran darah hati

dan ginjal

Sensitif thd reentrant arrhythmiadan penurunan ambang fibrilasi

ventrikel

Menghambat respon kardiovaskularterhadap katekolamin

AKIBAT DARI ASIDOSIS BERAT

12

Adrogue HJ, Nicolaos EM: Management of life-threatening Acid-Base Disorders,Review Article; NEJM 1998


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Memahami fisiologi cairanplasma dalam kerangkaterminologi Stewarts

approach


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Na+= 140 mEq/LCl-= 102 mEq/LSID = 38 mEq/L 140/1/2= 280 mEq/L

102/1/2 = 204 mEq/LSID = 76 mEq/L1

liter

liter

WATER DEFICIT

Diuretic

Diabetes Insipidus

Evaporasi

SID : 38 76 = alkalosis

ALKALOSIS KONTRAKSI

Plasma Plasma


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Na+ = 140 mEq/LCl- = 102 mEq/L

SID = 38 mEq/L

140/2 = 70 mEq/L102/2 = 51 mEq/L

SID = 19 mEq/L

1

liter

2

liter

WATER EXCESS

1 LiterH2O

SID : 38 19 = Acidosis

ASIDOSIS DILUSI

Plasma


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Efek terapi cairan terhadapkeseimbangan asam basa


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Na+= 140 mEq/LCl-= 102 mEq/LSID = 38 mEq/L

Na+= 154 mEq/LCl-= 154 mEq/LSID = 0 mEq/L1 liter 1 liter

PLASMA + NaCl 0.9%

SID : 38

Plasma NaCl 0.9%


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2 liter

ASIDOSIS HIPERKLOREMIK AKIBATPEMBERIAN LARUTAN Na Cl 0.9%

=

SID : 19 lebih asidosis

Na+= (140+154)/2 mEq/L= 147 mEq/L

Cl-= (102+ 154)/2 mEq/L= 128 mEq/L

SID = 19 mEq/L

Plasma


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Na+= 140 mEq/L

Cl- = 102 mEq/L

SID= 38 mEq/L

Cation+= 137 mEq/L

Cl-= 109 mEq/L

Laktat-= 28 mEq/L

SID = 0 mEq/L1 liter 1 liter

PLASMA + Larutan RINGER LACTATE

SID : 38

Plasma Ringer laktat

Laktat cepatdimetabolisme


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2 liter

=

Normal pH setelah pemberianRINGER LACTATE

SID : 34 lebih alkalosis dibanding jika

diberikan NaCl 0.9%

Na+= (140+137)/2 mEq/L= 139 mEq/L

Cl-= (102+ 109)/2 mEq/L = 105 mEq/L

Laktat- (termetabolisme) = 0 mEq/L

SID = 34 mEq/L

Plasma


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Na+= 140 mEq/L

Cl-= 130 mEq/L

SID =10 mEq/L

Na+= 165 mEq/L

Cl-= 130 mEq/L

SID = 35 mEq/L1 liter 1.025

liter

25 mEq

NaHCO3

SID : 10 35 : Alkalosis, pH kembali normal namun mekanismenya bukankarena pemberian HCO3

-melainkan karena pemberian Na+tanpa anion kuat ygtidak dimetabolisme seperti Cl-sehingga SID alkalosis

Plasma;asidosis

hiperkloremik

MEKANISME HIPERNATREMIA AKIBATPEMBERIAN NA-BIKARBONAT PADA

ASIDOSIS

Plasma + NaHCO3

HCO3cepatdimetabolisme


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Disain kristaloid seimbang

(Balanced) Pemberian infus NaCl dalam jumlah yang banyak

cenderung menyebabkan asidosis metabolik.

Untuk mengatasi hal ini, beberapa produk komersialkristaloid mendisain cairan yang lebih fisiologis ataudisebut cairan seimbang (balanced)

Cairan-cairan ini mengandung anion organik yang stabil

seperti laktat, glukonas dan asetat ,malate ( SID fluid >0 and < plasma SID)


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[mmol/l] NS Ringer RL RA RFundin Plasma

Na+ 154 147 130 130 140 142

K+ 4.0 4 4 4.0 4.5

Ca2+ 2.25 2.7 2.7 2.5 2.5

Mg2+ 1.0 1.0 0.85

Cl- 154 156 108.7 108.7 127 103

HCO3 24

Lactate- -- -- 28.0 -- -- 1.5

Acetate- -- -- -- 28.0 24.0

Malate2- -- -- -- -- 5.0

BEpot -24 -24 3.0 2.5 0 0 2

Tonicity

[mOsm/l]

[mOsm/lkg)

304

286

309 273

256

273.4

256

304

286

308

288

Electrolyte balance like in human plasma

=> physiological composition closely

resembling humanplasma needed

Conventional infusion solutions can produce

a number of corrective effects

both unwanted and unknown.

Ringerfundin does not

affect electrolyte

equilibrium

Balance solution - Plasmalike electrolytes


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R. Zander, Fluid Managemen

RL and RA are more

hypotonic compare to

NaCL 0.9% & RF


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Disain koloid seimbang(Balanced)


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Colloid HES in different solutions

Note

especially the

differences insodium and

chloride

content!

HES 130 in 0.9% saline:

Venofundin Bbraun & Voluven


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Na+= 142 mEq/L

Cl- = 103 mEq/L

SID= 39 mEq/L

Na+= 154 mEq/L

Cl-= 154 mEq/L

SID = 0 mEq/L1 L 1 L

PLASMA + Coloid-unbalanced (NaCl)

Plasma NaCl

Na+= (142 + 154)/2 = 147

Cl- = (103+154)/2 = 128

SID= 19 mEq/L

SID : 19 acidosis


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Na+= 142 mEq/L

Cl- = 103 mEq/L

SID= 39 mEq/L

Cation+= 147 mEq/L

Cl-= 118 mEq/L

Malate = 5 mEq/L

Acetat-= 24 mEq/L

SID = 29 mEq/L1 L 1 L

PLASMA + Coloid-balanced (Tetraspan)

Plasma BalancedColloidNa+= (142 + 147)/2 = 144

Cl- = (103+118)/2 = 110

Ac&Mal metabolisme)= 0

SID= 34 mEq/L

SID : 34

Acetat &malate cepatdimetabolisme


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Syok Hipovolemik

Tekanan Darah

CardiacOutput /

CO

IsiSekuncup /

SV

Kontraktilitas Beban Akhir

Denyut Jantung

TahananPembuluh

Sistemik (SVR)

Beban Awal


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Class I Class II Class III Class IV

Blood loss Up to 750 750-1500 1500-2000 >2000

Blood loss

( % EBV)

Up to 15% 15-30% 30-40% >40%

Pulse rate 100 >120 >140

Blood

pressure

Normal Normal Decrease Decrease

Pulse

pressure

Normal or

decrease

Decrease Decrease Decrease

Respiratory

rate

14-20 20-30 30-35 >35

Urineoutput

>30 20-30 5-15 No UO

CNS/

mental status

Slightly anxious Mildly anxious Anxious and

confused

Confused and

lethargic

Fluid

replacement

crystalloid crystalloid Crystalloid/

colloid

Crystallloid/

colloid


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Intravascular volume evaluation

Static evaluation Dynamic evaluation

Technique proposed to evaluate

hypovolemic

Overt hypovolemic Masking

hypovolemic

Fluid Challenge

A method assessing

responsiveness to fluid infusion

Signs of dehydrationDiminished skin turgor

Thirst

Dry mouth

Dry axillae

Hypernatremia, hyperproteinemia,

elevated hemoglobin/hematocrit

Circulatory signs of

hypovolemiaTachycardia

Arterial hypotension (severe cases)

Increased serum lactate (severe

cases)

Decreased toe temperature

Decreased renal perfusionConcentrated urine (low urine

sodium concentration, high urine

osmolarity)

Increased blood urea nitrogen

relative to creatinine concentration

Persistent metabolic alkalosis


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WHAT IS A FLUID CHALLENGE?RESERVED FOR HEMODYNAMICALLY UNSTABLE

PATIENTS

Three Major advan tages :

Quantization of the cardiovascular response during volume

infusion

Prompt correction of fluid deficits

Minimizing the risk of fluid overload and its potentially adverse

effects, especially on the lung


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INITIAL FLUID CHALLENGE

Weil and Henn ing (Several decades ago)

3 mmHg PAOPO

(2 mmHg CVP) Infusion was continued

Infusion was interrupted3-7 mmHg PAOPO

(2-5 mmHg CVP)

2-5 Rules Guided by Central Venous Pressure (CVP)2-5 Rules Guided by Pulmonary Artery Occlusions Pressure (PAOP)

reevaluated after 10-min wait

Infusion was stopped 7 mmHg PAOPO

( 5 mmHg CVP)

The Protoco l may be updated and even simpl i f ied


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MODIFIED FLUID CHALLENGEBased Largely on Clinical Experience and Published Literature

Type of fluid Rate of FluidAdministration

Goal To Be

Achieved

Safety Limit

Four Decision Phase


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MODIFIED FLUID CHALLENGE

Type of fluid

CrystalloidColloid

The molecules retained withinintravascular for longer intervals

More rapid completion of the challenge

Relative expensive Cost

Mildly hypotonic can exacerbatecerebral edema in brain injury patients

Low Cost

Album in, Starch, Gelat insLactate, Salt Solu ion s

No ideal intravenous fluid in all clinical settings

Choice is best made

contingent to:

Underlying disease

Type o fluid that has been lost,

The severity of circulatory failure

Serum albumin concentration,

Risk of Bleeding


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MODIFIED FLUID CHALLENGE

Safety Limit

Pulmonary

Edema due to

Congestive

Heart Failure

(CHF)

Most serious

complication of fluid

infusion

Guide by intermi t tent or cont inuou s Indicators

Pulmonary artery occlusion pressure (more direct)

Central Venous Pressure

Fluid Load 100 or 200 mL every 10 min


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Principles Management of

Electrolyte Imbalance Implies an underlying disease process

Treat the electrolyte change, but seek the

cause

Clinical manifestations usually not specific to

a particular electrolyte change, e.g., seizures,

arrhythmias


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Principles Management of

Electrolyte Imbalance Clinical manifestations determine

urgency of treatment, not laboratory

values

Speed and magnitude of correction

dependenton clinical circumstances

Frequent reassessment of electrolytes

required


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Hyponatremia

A low serum Na does not tell us whether

total extracellular Na is increased,

decreased,or normal It only tells us that there is excess water

relative to Na

Most cases of hyponatremia are causedby impaired water excretion in the

presence of continued water intake.


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Hyponatremia

History

Causes of ECFV depletion (vomiting,

diarrhea)?edematous states

Medications

Other underlying systemic diseases (SIADH) CNS diseases, pulmonary diseases, malignancy,

drugs


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Hyponatremia

Acute, symptomatic hyponatremia

Correct no faster than 1 mEq/L per hour for

the first 6-8 mEq/LNo more than 10-12 mEq/L in first 24 hours

5% saline is almost never needed

Calculate the Na deficit Na mEq = ([Na desired] - [Na measured]) X TBW

TBW = .5 or .6 X weight in KG


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Hypernatremia

Results from a deficit of water

Loss of water

Failure to adequately replace the water lossLook thoroughly for alterations in neurological

status that are causing inadequate water

intake

Water loss is extra-renal or renal

Rarely iatrogenic (administration of

hypertonic saline or NaHCO3)


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Hypernatremia

Osmotic diuresis (urine Osm > 300)

the excretion of the osmotic load obligates a

certain water losspoorly controlled diabetes, mannitol

administration, protein catabolism with urea

Diabetes Insipidus (urine Osm < 150) inability of the kidney to concentrate urine due

to absence of ADH (central) or

unresponsiveness to ADH (nephrogenic)


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Hypernatremia

Diagnosis

Reason for water loss or sodium gain?

Reason for inadequate water intake? Is polyuria present? (urine volume > 3L/24hrs)

What is the spot urine Osm?

Response to vasopressin?


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Hypernatremia

Treatment

Severe ECFV depletion is the priority and

should be corrected with NS first.

Subsequent fluid replacement can behypotonic

Major complication of overly rapid correction

is cerebral edema

Safe rate is no more than .5- 1 mEq/L per

hour

Should take 36-72 to hours to completely

correct


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Hypernatremia

Treatment

Calculate the water deficit

H2O deficit = TBW X ([Na meas]- [Nades])/[Na des]

Important to take into account ongoing losses

insensible losses .5 - 1 liter/24 hours

with fever, these losses increase by 60-80ml/24

hrs for each degree Farenheit


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Hypokalemia

Neuromuscular manifestations (weakness,

fatigue, paralysis, respiratory dysfunction)

GI (constipation, ileus) Nephrogenic DI

ECG changes (U waves, flattened T

waves)

Arrhythmias


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Hypokalemia

Spurious hypokalemia

Marked leukocytosis

A dose of insulin right before the blood draw

Redistribution hypokalemia

Alkalosis (K decreases .3 for every .1

increase in pH) Increased Beta2adrenergic activity

Theophylline toxicity

Familial


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Hypokalemia

Renal losses

metabolic acidosis

RTA Type I and II DKA

Carbonic anhydrase inhibitor therapy

Ureterosigmoidostomy

No acid-base disorder

Mg deficiency

Drugs


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Hyperkalemia

Severe hyperkalemia is a medical

emergency

Neuromuscular signs (weakness,ascending paralysis, respiratory failure)

Progressive ECG changes (peaked T

waves, flattened P waves, prolonged PRinterval, idioventricular rhythm and

widened QRS complex, sine wave

pattern, V fib)


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Hyperkalemia

Etiologyrenal

failure, transcellular

shifts, cell death,

drugs,

pseudohyperkalemia

Manifestations

cardiac,

neuromuscular


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Hyperkalemia

Impaired potassium secretion

Aldosterone deficiency

adrenal failure Syndrome of hyporeninemic hypoaldosteronism

(SHH)

tubular unresponsiveness

Renal failure GFR < 10 -20% of normal


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Hyperkalemia

Treatment

Stop potassium!

Get and ECGHyperkalemia with ECG changes is a medical

emergency


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Hyperkalemia

Treatment

First phase is emergency treatment to

counteract the effects of hyperkalemia IV Calcium

Temporizing treatment to drive the potassium

into the cells

glucose plus insulin

Beta2agonist

NaHCO3


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Hyperkalemia

Treatment

Therapy directed at actual removal of

potassium from the body sodium polystyrene sulfonate (Kayexalate)

dialysis

Determine and correct the underlying cause


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THANK YOU

Fluid Therapy,Acid-Base and Electrolyte Imbalance(Dr.tini)

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Transcript of Fluid Therapy,Acid-Base and Electrolyte Imbalance(Dr.tini)