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GANGGUAN KESEIMBANGAN
ASAM BASA, CAIRAN, DAN
ELEKTROLIT
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 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.
Buffer systems
Respiration
Renal function
Maintain tight control within range 7.35 7.45
The Central Role of the Carbonic AcidBicarbonate Buffer System in the Regulation of
Plasma pH
Figure 27.11a
The Central Role of the Carbonic AcidBicarbonate Buffer System in the Regulation of
Plasma pH
Figure 27.11b
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
Acid-Base Disorders
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
Figure 27.12a
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
Figure 27.13
1. Measure pH
high pH
Respiratory alkalosis
low pH
Metabolic acidosis
2. Determine AG
Increased Gap
ketoacidosis
lactic acidosis
uremia
Normal Gap
Renal tubular acidosis
GI disease
Acid intake
Workup of normal AG
metabolic acidosis
1. Serum K
Decreased
2. Urinary pH
pH >5.5
Distal RTA
Increased or Normal :
Early uraemic acidosis
Obstructive nephropathy
Mineralocorticoid deficiency
Infusion / ingestion: HCl, NH4Cl
pH<5.5
Proximal RTA
Acute Diarrhea
Metabolic Alkalosis
Figure 27.14
ECV
Aldosterone
Bicarbonate
Reabsorbtion
H+secretion
Alkalosis
Alkalosis
KCl
H+ Shift
into cells
ECF
Contraction
AKALOSIS
Shift H+
Into cells
Proximal Tubule
Bicarbonate
Reabsorbtion
Acid
Urine
Exchange Na for
H in Distal
Tubule
Exchange Na for
K in Distal
Tubule
Aldosterone
1. measure pH
low pH
Respiratory acidosis
high pH
Metabolic alkalosis
2. Assess ECV
a. history
b. exam
c. urine Na
ECV depletion
a. GI losses
b. Diuretics
c. severe K depletion
ECV normal
a. aldosteronism
b. alkali intake
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.
Pulmonary disease
Chronic bronchitis, Chronic emphysema, Asthma, Pneumonia
Depression of respiratory
center
Strokes
Tumors
Encephalitis
Drugs : narcotics
sedatives
tranquilizers
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
Figure 27.15
KESIMPULAN
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
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
Asidosis metabolik
Alkalosis metabolik
Asidosis respiratorik akut
Alkalosis respiratorik akut
Asidosis respiratorik kronik
Alkalosis respiratorik kronik
KOMPENSASI
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
1. Biasanya patologik
2. Sering pd
inkompatibilitas
ABO rhesus
3. Bukan sepsis
4. Inkompatibilitas
golongan darah
yang lain
5. Defisiensi G6PD
6. Defek membran
eritrosit (sferositosis
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
Konjugasi
oleh hati
Produksi seperti
pada perdarahan
atau hemolitik
intravaskuler
Ambilan
oleh hati
PATOGENESIS
Gangguan
ekskresi
bilirubin
Sirkulasi
enterohepaptik
Gangguan aliran
empedu pada
kolestasis
Merckmanual. Neonatal hyperbilirubinemia. 2009. Diunduh dari: http://www.merckmanuals.com. Pada tanggal 29 Desember 2010
PATOFISIOLOGI
Bilirubin unconjugated >>>
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
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.
>14,6
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
Hemolitik isoimun
2. Defisiensi G6PD
3. Asfiksia
4. Letargi
5. Suhu tubuh tidak stabil
6. Sepsis
7. Asidosis
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.
SEPSIS NEONATORUM
Terima kasih