fluid therapy,acid-base and electrolyte imbalance(dr.tini)
TRANSCRIPT
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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