GANGGUAN KESEIMBANGAN

ASAM BASA

ARINA NURFIANTI
 LEVEL NORMAL
Parameter Reference range Reference point
pH 7.35-7.45 7.40
PCO2 33-44 mm Hg 40 mm Hg

PO2 75-105 mm Hg
HCO3- 22-28 mEq/L 24mEq/L
Anion gap 8-16 mEq/L 12 mEq/L
Osmolar gap <10 mOsm/L
 REFERENGE
Primary Disturbance pH HCO3- PCO2 Compensation

Respiratory acidosis <7.35 Compensatory Primary Acute: 1-2 mEq/L increase in HCO3- for
increase increase every 10 mm Hg increase in PCO2
Chronic: 3-4 mEq/L increase in HCO3-
for every 10 mm Hg increase in PCO2
Respiratory alkalosis >7.45 Compensatory Primary Acute: 1-2 mEq/L decrease in HCO3- for
decrease decrease every 10 mm Hg decrease in PCO2
Chronic: 4-5 mEq/L decrease in HCO3-
for every 10 mm Hg decrease in PCO2
Metabolic acidosis <7.35 Primary Compensatory 1.2 mm Hg decrease in PCO2 for every 1
decrease decrease mEq/L decrease in HCO3-
Metabolic alkalosis >7.45 Primary increase Compensatory 0.6-0.75 mm Hg increase in PCO2 for
increase every 1 mEq/L increase in HCO3-
, PCO2 should not rise above 55 mm Hg
in compensation
• low PH, high CO2, high HCO3 = RESP. ACIDOSIS

high PH, low CO2, low HCO3 = RESP. ALKALOSIS

low PH, low CO2, low HCO3 = METABOLIC ACIDOSIS

high PH, high CO2, high HCO3= METABOLIC ALKALOSIS

 PENGKAJIAN
• History – riwayat penyakit, trauma, medications, poisons, toxins
• Pemeriksaan Fisik
• Laboratory studies – perubahan dari nilai normal
• Compensation – pengkajian pada masalah awal dan kompensasinya
 Respiratory acidosis
PCO2 tinggi
Acute or chronic
Penyebab
 Penyebab dasar: HIPOVENTILASI
 kelebihan CO2 saat inspirasi
(rebreathing of CO2-)
 Penurunan ventilasi alveolar
(depresi SSP, gangguan otot pernafasan, apnea, henti
jantung akut, overdosis terapi opiat-analgesik-sedatif)
COPD, pneumonia, edema paru akut
 increased production of CO2
(hypercatabolic disorders)
 Penanganan asidosis respiratorik
• Memulihkan ventilasi efektif SEGERA
• Mengatasi penyebab yg mendasari
• PO2 dinaikkan sampai bts minimum
• Pemberian terapi O2 bukan aliran tinggi/
aliran rendah
• Ventilasi mekanik jika tidak ada riwayat
hiperkapnia
 Respiratory alkalosis
PCO2 kurang dari normal
Acute or chronic
Penyebab
 Penyebab dasar: HIPERVENTILASI alveolar/ eksresi
CO2 berlebih
 Peningkatan ventilasi alveolar
(stres, nyeri berat, hipoksemia, gagal jantung, latihan
fisik berat dan berlebih, cedera kepala, tumor otak)

Sepsis
Sirosis hepatis
 Penanganan alkalosis respiratorik

• Koreksi penyebab
• Menurunkan ventilasi melalui alat ventilator
• Mengurangi kecemasan
• Bernafas kembali pada kantong yg dirapatkan
pada hidung mulut
• Rebreather mask
 Metabolic acidosis
Semua nilai parameter TURUN/ RENDAH
Penyebab
 Selisih anion meningkat/ peningkatan produksi H+
(ketoacidosis, asidosis laktat misalnya pada syok
kardiogenik, renal failure, intoksikasi metanol)
 Selisih anion normal
(diare, ileostomi, pemberian cairan Iv secara cepat dan
berlebih, hiperkalemia)
Perhatikan nilai Lab. Ureum dan kreatinin tinggi
 Penanganan asidosis metabolik

• Atasi penyebab
• Koreksi ginjal
• Pemberian insulin
• Pemberian cairan iv RL
• Pemberian Natrium bikarbonat (NaHCO3) i,.v
(perhatikan risiko komplikasi alkalosis
metabolik)
• HEmodialisis
 Metabolic alkalosis

Semua parameter NAIK

Causes (2 ways to organize)
 loss of H+ from ECF via kidneys (diuretics) atau saluran
cerna (muntah, penyedotan nasogastrik berlebih)
 Peningkatan alkali akibat kelebihan natrium bikarbonat
or
 addition of base to ECF (milk-alkali syndrome)- antasida
 Cl- menurun (muntah kronis, intoksikasi)
 K+ menurun (hiperaldosteron)
 Hipoalbuminemia
 Penanganan alkalosis metabolik
• Mengatasi penyebab
• Infus iv + penambahan KCL
• Asetazolamid pd pasien dengan pemberian
diueretik
• Suplemen K+
 Racid acute
A 65-year-old man with a history of emphysema comes to the physician with a
3-hour history of shortness of breath.
pH 7.18
PO2 61 mm Hg

PCO2 58 mm Hg
HCO3- 26 mEq/L
History suggests hypoventilation, supported by increased PCO2 and lower than
anticipated PO2.
Respiratory acidosis (acute) due to no renal compensation.
 Ralk acute
A 17-year-old woman is brought to the physician with a 3-hour history of
epigastric pain and nausea. She admits taking a large dose of aspirin. Her
respirations are full and rapid.
pH 7.57
PO2 104 mm Hg
PCO2 25 mm Hg
HCO3- 23 mEq/L
History suggests hyperventilation, supported by decreased PCO2.
Respiratory alkalosis (acute) due to no renal compensation.
 Ralk chronic
A 81-year-old woman with a history of anxiety is brought to the physician with a
2-hour history of shortness of breath. She has been living at 9,000 ft elevation
for the past 1 month. Her respirations are full at 25/min.
pH 7.44
PO2 69 mm Hg
PCO2 24 mm Hg
HCO3- 16 mEq/L
History suggests hyperventilation, supported by decreased PCO2.
Respiratory alkalosis (chronic) with renal compensation.
 Macid high AG
A 75-year-old man with severe congestive heart failure is brought to the
emergency department. He is on no medication. His respirations are 24/min
and blood pressure is 80/50 mm Hg. He has decreased urine output; his
baseline creatinine concentration has been 1.6 mg/dL.
pH 7.19 Na+ 135 mEq/L
PO2 80 mm Hg K+ 4.0 mEq/L
PCO2 20 mm Hg Cl- 97 mEq/L
HCO3- 8 mEq/L CO2, total 8 mEq/L
Lactate 20 mEq/L Urea 54 mg/dL
Creatinine 2.5 mg/dL
History suggests congestive heart failure (poor perfusion).
Metabolic acidosis with appropriate respiratory compensation.

Jika