dr.

Agustyas Tjiptaningrum, SpPK

GANGGUAN KESEIMBANGAN
ASAM BASA, CAIRAN, DAN
ELEKTROLIT
Acid Base Disorders
 ACID-BASE REGULATION

The body attempts to maintain a pH

between 7.35 and 7.43 (hydrogen ion
concentration between 35 and 45 nmol/L.
This is achieved despite considerable
variation in acid-base intake
Elimination of volatile acids

Volatile hydrogen ion are eliminated by

the lungs as CO2 based on:

H+ + HCO3- H2CO3 CO2 + H2O

 Sources of nonvolatile acids
Diet, about 30 mEq of H ion is added to the
body daily. (this can increase with a very
high animal protein intake)
Incomplete metabolism, about 30mEq/day
(ketoacids,betahydroxybutyrate etc)
Stool loss of Bicarbonate, around 20mEq
bicarbonate is lost in stools daily.
Elimination of acid-base
Lungs.
The lungs eliminate a large amount of volatile
acid as CO2.This can be greatly increased or
modestly decreased if the lungs are normal.
Kidneys.
Acid excretion and alkali excretion Normally
the kidneys are called on to excrete 70 to 100
mEq acid/day. This can be reduced to 0 or
increased to fourfold. If faced with an alkaline
load,the kidneys can excrete hundreds mEq of
bicarbonate.
 Abnormal States
Lungs: Abnormalities can lead to reduced
CO2 or too much CO2.
Kidneys: Deficient or excess H ion excretion.
Excess HCO3 regeneration or loss.
Metabolic abnormalities: Diabetes, poor
tissue perfusion, anaerobic metabolism.
Gastrointestinal abnormalities: Vomiting,
diarrhea.
 Disturbances of Acid-base Balance

Buffer systems
Respiration
Renal function
Maintain tight control within range 7.35 7.45

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

 The Central Role of the Carbonic Acid-
Bicarbonate Buffer System in the Regulation of
Plasma pH

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 27.11a
 The Central Role of the Carbonic Acid-
Bicarbonate Buffer System in the Regulation of
Plasma pH

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 27.11b
Measurements and Calculations

Hydrogen concentration (pH)

Bicarbonate concentration (HCO3)
pCO2
Anion Gap (AG).
The bodys buffer system.
Carbonic acid bicarbonate system

Hemoglobin

Protein
The Henderson Hasselbalch
equation
Clinically, the carbonic acid bicarbonate
system is most important. By applying
the law of mass action to the following
reaction:
CO2 + H2O H2CO3 H+ +HCO3-
one obtains the classic equation:
pH = 6.1 + log [HCO3] / pCO2
The Henderson Hasselbalch
equation
The classic equation:
pH = 6.1 + log [HCO3] / pCO2
The practical equation:
[H+] = 24 x pCO2 / [HCO3-]
pH = 7.40
[HCO3-] = 24 mEq/L
[H+] = 40 nmol/L
pCO2 = 40 mmHg
Specific Disturbances
Metabolic acidosis (a fall in pH and a
decrease in HCO3-)
Metabolic alkalosis (a rise in pH and an
increase in HCO3-)
Respiratory acidosis (a fall in pH resulting
from a primary increase in pCO2)
Respiratory alkalosis (a rise in pH from a
decrease in pCO2)
Figure 27.6 The Basic Relationship between PCO2
and Plasma pH

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 27.6
Acid-Base Disorders

Respiratory acid-base disorders

Result when abnormal respiratory function
causes rise or fall in CO2 in ECF
Metabolic acid-base disorders
Generation of organic or fixed acids
Anything affecting concentration of
bicarbonate ions in ECF

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Respiratory acid-base disorders

Respiratory acidosis
Results from excessive levels of CO2 in body
fluids
Respiratory alkalosis
Relatively rare condition
Associated with hyperventilation

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Compensation.
Metabolic disorders:
The pulmonary response will attempt to
correct the pH.
Respiratory correction occurs
immediately.
Respiratory disorders:
The kidneys regulates bicarbonate levels
It takes several hours to respond
 Respiratory Acid-Base Regulation

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 27.12a
 Respiratory Acid-Base Regulation

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 27.12b
Incomplete Compensation
When compensation fails to occur, it is
because of disease in that system.

This is then termed a mixed or combined

disorder
Anion Gap
In the blood, when measured, cations
seem to exceed anions in number. This
is due to the plasma proteins, the
difference amounts to about 10 12
mEq/L.

Anion Gap = [Na+] (Cl- + HCO3-)

Anion Gap
An increased AG always means a
metabolic acidosis is present.

An increased AG implies that the cause of

acidosis must be retention of some acid
other than HCl.
Metabolic Acidosis
Metabolic acidosis results from three
types of disorders:
excess acid load
decreased acid excretion by the
kidney
alkali (bicarbonate) loss
Metabolic acidosis
Normal AG (hyperchloremic metabolic acidosis)
A. Excess intake (HCl, NH4Cl)
B. Bicarbonate loss
1. GI tract
Diarrhea
Fistulas
2. Proximal renal tubular acidosis
C. Decreased renal acid secretion. (distal
renal tubular acidosis)
Metabolic acidosis
Increased AG
A. Ketoacidosis
1. Diabetes mellitus
2. Alcohol
B. Lactic acidosis (usually due to shock)
C. Poisons
D. Renal failure
Metabolic acid-base disorders
Major causes of metabolic acidosis are:
Depletion of bicarbonate reserve
Inability to excrete hydrogen ions at kidneys
Production of large numbers of fixed / organic
acids
Bicarbonate loss due to chronic diarrhea
Metabolic alkalosis
Occurs when HCO3- concentrations become
elevated
Caused by repeated vomiting
Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings
 The Response to Metabolic Acidosis

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 27.13
 Workup of metabolic acidosis.
low Bicarbonate

1. Measure pH

high pH low pH
Respiratory alkalosis Metabolic acidosis

2. Determine AG

Increased Gap Normal Gap

ketoacidosis Renal tubular acidosis
lactic acidosis GI disease
uremia Acid intake
 Workup of normal AG
metabolic acidosis
1. Serum K

Decreased Increased or Normal :

Early uraemic acidosis
Obstructive nephropathy
2. Urinary pH Mineralocorticoid deficiency
Infusion / ingestion: HCl, NH4Cl

pH >5.5 pH<5.5

Proximal RTA
Acute Diarrhea
Distal RTA
 Metabolic Alkalosis

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 27.14
Causes of metabolic alkalosis
HCl loss
a. Gastrointestinal
b. Increased urine acidification
Excess alkali intake
a. Alkali abuse
b. Treatment of acidosis
Severe potassium depletion
Primary causes of alkalosis
Vomiting/Diuretics
Vomiting/Diuretics

ECV HCl KCl

Aldosterone Bicarbonate H+ Shift

Reabsorbtion into cells

H+secretion

Alkalosis
Alkalosis
Secondary causes of alkalosis
K ECF
Depletion Contraction

AKALOSIS

Shift H+ Proximal Tubule

Into cells Bicarbonate
Reabsorbtion
Acid
Urine
Exchange Na for
H in Distal
Tubule Aldosterone
Exchange Na for
K in Distal
Tubule
Workup of metabolic alkalosis
elevated Bicarbonate

1. measure pH

low pH high pH
Respiratory acidosis Metabolic alkalosis

2. Assess ECV
a. history
b. exam
c. urine Na

ECV depletion ECV normal

a. GI losses a. aldosteronism
b. Diuretics b. alkali intake
c. severe K depletion c. severe K depletion
Respiratory disorders
Respiratory Acidosis
This disorder results from hypoventilation.
Because chemical buffering is limited.
Acute respiratory failure is associated with
severe acidosis with little increase in plasma
bicarbonate.
Chronic respiratory failure causes increased
renal generation of bicarbonate.
Causes of respiratory acidosis
Depression of respiratory center
Stroke, Tumors, Encephalitis, Drugs

Limitation of chest wall movement

Neuromuscular disorders, Trauma, Surgery, Fixation of ribs

Pulmonary disease
Chronic bronchitis, Chronic emphysema, Asthma, Pneumonia
Depression of respiratory
center
Strokes
Tumors
Encephalitis
Drugs : narcotics
sedatives
tranquilizers
Limitation of chest wall
movement
Neuromuscular disorder :
myasthenia gravis
Guillain Barr
tetanus
Trauma and surgery
Fixation of ribs
Pulmonary disease
Chronic bronchitis
Chronic emphysema
Asthma
Pneumonia
Respiratory alkalosis
This disorder results from hyperventilation due
to a variety of causes.
Acute hypocapnia causes release of H ions
from tissue buffers, this tends to minimize the
reduction of plasma bicarbonate.
Chronic hypocapnia stimulates renal adaptation
with reduced bicarbonate generation, thus
lowering plasma bicarbonate concentration.
Causes of respiratory
alkalosis
Direct stimulation of respiratory center.
Psychogenic, CNS disease, Sepsis, Hypermetabolic state,
Exercise, Liver failure, Drugs

Reflex stimulation of respiratory center.

Pneumonia, Pulmonary edema, Pulmonary fibrosis, Asthma,
Cyanotic heart disease

Excessive mechanical ventilation

Direct stimulation of respiratory
center
Psychogenic
CNS disease : stroke, encephalitis
Sepsis
Hypermetabolic state: fever, thyrotoxicosis.
Exercise
Liver faillure
Drugs: salicylates, ammonia, progesterone
Reflex stimulation of respiratory
center
Pneumonia
Pulmonary edema
Pulmonary fibrosis
Asthma
Cyanotic heart disease
 Detection of acidosis and alkalosis

Diagnostic blood tests

Blood pH
PCO2
Bicarbonate levels
Distinguish between respiratory and metabolic

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

 A Diagnostic Chart for Acid-Base Disorders

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 27.15
 Aging and Fluid, Electrolyte, and Acid-base
Balance

Reduced total body water content

Impaired ability to perform renal compensation
Increased water demands
Reduced ability to concentrate urine
Reduced sensitivity to ADH/ aldosterone
Net loss of minerals
Inability to perform respiratory compensation
Secondary conditions that affect fluid, electrolyte, acid-
base balance

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

 KESIMPULAN

Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

 KESIMPULAN
Terdapat 4 macam gangguan keseimbangan asam basa :
1. Asidosis metabolik pH , [HCO3-] akibat keluarnya bicarbonat dari tubuh
atau penambahan hidrion yg akan bereaksi dg bicarbonat asam karbonat
CO2 dan H2O
2. Alkalosis metabolik pH , [HCO3-] akibat hilangnya HCL mll muntah atau
sekresi lambung
3. Asidosis respiratorik pH , PCO2 hipoventilasi
4. Alkalosis respiratorik pH , PCO2 hiperventilasi
Tubuh akan mengkompensasi setiap gangguan keseimbangan asam basa

GANGGUAN METABOLIK
Baik asidosis maupun alkalosis respon paru
Asidosis hiperventilasi PCO2 , [H+]
Alkalosis hipoventilasi PCO2 , [H+] kembali N kompensasi ini terba
tas karena dapat menyebabkan hipoksia (PO2 <<) memicu kembali ventila
si (saat PO2 60 mmHg)
 KESIMPULAN
GANGGUAN RESPIRATORIK
Kompensasi oleh ginjal pengaturan kadar bikarbonat
Asidosis respiratorik produksi dan retensi HCO3-
Alkalosis respirarorik ekskresi HCO3-, [HCO3-] plasma pH N
Kompensasi oleh ginjal berjalan lambat (beberapa jam)
GANGGUAN KOMPENSASI
Asidosis metabolik Setiap 1 mEq [HCO3-], PCO2 1-1.3 mmHg
Alkalosis metabolik Setiap 1 mEq [HCO3-], PCO2 0.6 mmHg
Asidosis respiratorik akut Setiap 1 mm PCO2 , [HCO3-] 0.1 mEq
Alkalosis respiratorik akut Setiap 1 mm PCO2 , [HCO3-] 0.2 mEq
Asidosis respiratorik kronik Setiap 1 mm PCO2 , [HCO3-] 0.35 mEq
Alkalosis respiratorik kronik Setiap 1 mm PCO2 , [HCO3-] 0.5 mEq

Bila kompensasi tidak komplet gangguan asam basa

Anion Gap perbedaan kation mayor (sodium) dan anion mayor (Cl dan bika
rbonat)
AG asidosis metabolik retensi asam selain HCL
PEMERIKSAAN LABORATORIUM
PADA NEONATUS
Ikterus neonatorum
Ikterus neonatorum secara fisiologis dapat terjadi
akibat:
Peningkatan produksi bilirubin karena pemecahan
eritrosit masa janin (fetal erythrocyte) karena
masa hidup fetal erythrocyte memendek
Kapasitas ekskresi hepar untuk bilirubin ini masih
rendah pada neonatus karena masih sedikitnya jumlah
protein yang mengikat bilirubin untuk dibawa masuk
ke hepar dan masih rendahnya aktivitas enzim
glucoronyl transferase
 IKTERUS NEONATORUM

Kuning pada bayi baru lahir akibat penimbunan bilirubin

unconjugated pada kulit dan sklera

ETIOLOGI

ONSET < 24 JAM ONSET > 10 HARI

1. Biasanya patologik ONSET 24J-10 HARI 1. Conjugated
2. Sering pd 1. Fisiologis hyperbilirubinemia
inkompatibilitas 2. Sepsis hepatitis neonatal
ABO rhesus 3. Hemolisis idiopatik, TORCH, VHB,
3. Bukan sepsis 4. Polisitemia malformasi condenital
4. Inkompatibilitas 5. Perdarahan spt atresia biliar, defisiensi
golongan darah 6. Peningkatan AAT-1, atau GSD tipe IV
yang lain sirkulasi 2. Sepsis
5. Defisiensi G6PD enterohepatik 3. Hipotiroid
6. Defek membran pada obstruksi 4. Hemolisis
eritrosit (sferositosis usus 5. Ikterik akibat ASI
herediter
Hansen TWR. Jaundice, neonatal. 2010. Diunduh dari: http://emedicine/medscape.com. Pada tanggal 29 Desember 2010.
Statewide Maternity and Neonatal Clinical Guidelines Program. Neonatal jaundice: prevention, assessment, and management. 1st ed. Queensland: Queensland Government; 2009.p5-9 6
 Produksi seperti
pada perdarahan
atau hemolitik
Konjugasi intravaskuler
Ambilan
oleh hati oleh hati

PATOGENESIS

Gangguan
ekskresi Sirkulasi
bilirubin enterohepaptik
Gangguan aliran
empedu pada
kolestasis

Merckmanual. Neonatal hyperbilirubinemia. 2009. Diunduh dari: http://www.merckmanuals.com. Pada tanggal 29 Desember 2010
 PATOFISIOLOGI
Bilirubin unconjugated >>>

Kapasitas albumin untuk

mengikat terbatas

Bilirubin unconjugated bebas

(larut dalam lipid membran sel)

Menembus sawar otak

Neurotoksik

Kern icterus

Merckmanual. Neonatal hyperbilirubinemia. 2009. Diunduh dari: http://www.merckmanuals.com. Pada tanggal 29 Desember 2010
Hansen TWR. Jaundice, neonatal. 2010. Diunduh dari: http://emedicine/medscape.com. Pada tanggal 29 Desember 2010
 GEJALA KLINIK
Bila terdapat bilirubin encephalopathy terdapat gejala:
Hipotonia
Letargi
Kejang
koma
PEMERIKSAAN FISIK
Ikterik pada sklera dan kulit
Penilaian derajat ikterik menggunakan Kramers rules

( mg/dL) 5,9 8,8 11,7 14,6 >14,6

Hansen TWR. Jaundice, neonatal. 2010. Diunduh dari: http://emedicine/medscape.com. Pada tanggal 29 Desember 2010.
Statewide Maternity and Neonatal Clinical Guidelines Program. Neonatal jaundice: prevention, assessment, and management. 1st ed. Queensland: Queensland Government; 2009.p5-9.
American Academic of Pediatrics. Clinical practice guidelines:management of hyperbilirubinemia in the newborn infant 35 or more weeks gestation. Pediatrics. 2004;114(1):297-316.
 PEMERIKSAAN LABORATORIUM

1.KIMIA:
Bilirubin total, direk, dan indirek
2. HEMATOLOGI
Hematologi lengkap
Gambaran darah tepi
Retikulosit
Golongan darah ABO/rhesus
Coombstest
G6PD
3. URINALISIS
4. KULTUR bila dicurigai sepsis

Hansen TWR. Jaundice, neonatal. 2010. Diunduh dari: http://emedicine/medscape.com. Pada tanggal 29 Desember 2010.
Statewide Maternity and Neonatal Clinical Guidelines Program. Neonatal jaundice: prevention, assessment, and management. 1st ed. Queensland: Queensland Government; 2009.p5-9.
American Academic of Pediatrics. Clinical practice guidelines:management of hyperbilirubinemia in the newborn infant 35 or more weeks gestation. Pediatrics. 2004;114(1):297-316.
 DIAGNOSIS
Diagnosis ditegakkan berdasarkan anamnesis, pemeriksaan fisik, dan
pemeriksaan laboratorium
Indikasi pemeriksaan billirubin serum :
1. Ikterik tampak pada 24 jam pertama neonatus
2. Ikterik tidak sesuai dengan umur neonatus
3. Keraguan derajat ikterus, terutama kulit gelap
4. Ikterik berkelanjutan hingga 2 minggu (aterm) dan > 3 minggu (preterm)
5. Ikterus pada neonatus dengan kondisi klinis yang tidak baik
Mencari faktor risiko :
1. Hemolitik isoimun
2. Defisiensi G6PD
3. Asfiksia
4. Letargi
5. Suhu tubuh tidak stabil
6. Sepsis
7. Asidosis
8. Kadar albumin serum <3 g/dL (bila diperiksa)
Hansen TWR. Jaundice, neonatal. 2010. Diunduh dari: http://emedicine/medscape.com. Pada tanggal 29 Desember 2010.
Statewide Maternity and Neonatal Clinical Guidelines Program. Neonatal jaundice: prevention, assessment, and management. 1st ed. Queensland: Queensland Government; 2009.p5-9.
American Academic of Pediatrics. Clinical practice guidelines:management of hyperbilirubinemia in the newborn infant 35 or more weeks gestation. Pediatrics. 2004;114(1):297-316.
 Risiko Neonatus

Resiko sedang
1. Neonatus cukup bulan
(>38 minggu) dengan
faktor risiko
2. Neonatus kurang bulan
(35-37 6/7 mgg) sehat

American Academic of Pediatrics. Clinical practice guidelines:management of hyperbilirubinemia in the newborn infant 35 or more weeks gestation. Pediatrics. 2004;114(1):297-316.
DETEKSI HIPOTIROIDISME PADA NEONATUS

Prevalensi hipotiroidism pada neonatus sekitar 1

dalam 3000-5000
Deteksi dini hipotiroidism pada neonatus sangat
penting untuk mengeliminasi retardasi mental berat
akibat defisiensi hormon tiroid
Pemeriksaan untuk skrining hipotiroid pada neonatus
adalah TSH dan T4 darah
Bahan pemeriksaan dry blood spot atau darah tali
pusat
Pada bayi dengan berat badan lahir yang sangat
rendah disarankan pengulangan tes pada 2
minggu dan 4-6 minggu berikutnya untuk mendeteksi
late-onset transient hypothyroidism
Henryjs clinical laboratory
DETEKSI HIPOTIROIDISME PADA NEONATUS

Nilai rujukan pada initial TSH tali pusat <10mIU/L

bila nilainya 10-20 mIU/L maka dilakukan
pengulangan pemeriksaan 2-6 minggu kemudian
Bila TSH pada blood spot >20 mIU/L maka perlu
dilakukan evaluasi endokrin untuk menegakkan
diagnosis hipotiroid neonatus
False positive pada pem T4 dapat terjadi prematur
atau kelainan kongenital berupa tidak terdapatnya
TBG sehingga pemeriksaan T4 saja tidak cukup
untuk menegakkan diagnosis hipotiroid tapi harus
disertai dengan pemeriksaan TSH

Henryjs clinical laboratory

 SEPSIS NEONATORUM

Sepsis terjadi bila terdapat bakteriemia

Pemeriksaan laboratorium pada sepsis neonatorum
adalah:
Pemeriksaan darah lengkap neutrofilia shift to the
left
IT ratio yaitu ratio antara Immature-Total
Neutrophil normal <0,2
CRP C reactive protein peningkatan CRP
Procalcitonin Procalcitonin diexpresikan pada
keadaan infeksi lebih spesifik untuk diagnosis sepsis
Kultur darah 2,5 mL darah dikultur dgn BHI atau
BacTek/BacT alert 5 hari diinkubasi diliat
pertumbuhan kuman dan identifikasi
Terima kasih