Acid-Base Balance

Keseimbangan asam basa:

 Homeostasis cairan tubuh tergtg pada
pH darah arterial normal
 pH diatur oleh carbonic acid (H2CO3)
and bicarbonate (HCO3-) ekstraseluler
 Asam mrpkan molekul yang melepaskan
dlm btk ion H+
 Basa, mrpkn molekul yg menerima ion
H+
 Asam kuat atau basa kuat : senyawa yg
dpt terdisosiasi sempurna dalam
larutan/air:
- HCl, NaOH, and H2SO4

 Asam lemah/basa lemah: terdisosiasi

parsial : H2CO3, C3H6O3, and CH2O
 Regulasi pH:
 Homeostasis pH dikontrol melalui sistem
Protein buffering & intraseluler ekstraseluler
Buffer
system
 Pernapasan: menghilangkan CO2
HCO3-  Ginjal: melestarikan HCO3-dan
Buffer
system menghilangkan ion H +
 Elektrolit: komposisi ekstraseluler (ECF) &
K+ - H + intraseluler cairan (ICF)
Exchange
 -ECF dipertahankan pada 7,40

Mekanisme kontrol respirasi:
 Bekerja cepat dalam beberapa menit utk
kontrol pH, maksimal 12-24 jam
 Hanya efektif 50-75%
 Kelebihan CO2 dan H dalam darah akan lsg
memberi sinyal ke pusat respirasi otak
 CO2 melewati barier darah-otak bereaksi
dgn H2O membentuk H2CO3
 H2CO3 dihidrolisis menjadi H+ & HCO3- , H
akan menstimulasi peningkatan atau
penurunan respirasi
 Mekanisme kontrol oleh ginjal
:
 Tidak bekerja secepat sist respirasi, bisa
selama beberapa hari utk mengembalikan
pH atau mendekati normal
 Mengatur pH melalui ekskresi asam atau
alkalin urin; mengekskresikan kelebihan H
dan membentuk atau mereabsorpsi HCO3-
 Menurunkan keasaman urin dengan
ekskresi asam ke EC dan menurunkan
kebasaan urin dengan ekskresi basa
H+ elimination
& HCO3-
conservation
 Mechanisms of Acid-Base
Balance:
 Rasio HCO3-Base ke H2CO3 volatile menentukan
pH
Phosphate
 Konsentrasi H2CO3 volatile diatur dengan
Buffer
system mengubah tingkat & kedalaman respirasi
 Konsentrasi plasma HCO3-diatur oleh ginjal
melalui 2 proses: reabsorpsi yang disaring
Ammonia
Buffer
HCO3-& generasi HCO3 baru-, atau
system eliminasi H + buffered oleh sistem Tubular
untuk mempertahankan pH luminal
setidaknya 4,5

Gangguan metabolik:
 Alkalosis: ditinggikan HCO3-(> 26 mEq/L)
 Penyebab termasuk: Cl-penipisan (muntah,
berkepanjangan nasogastric pengisap),
Cushing sindrom, K + kekurangan, transfusi
darah besar-besaran, menelan antasid
Heartburn, dll.
 Asidosis: penurunan HCO3-(< 22 mEq/L)
 Penyebab termasuk: DKA, shock,
keracunan darah, gagal ginjal, diare, salisilat
(aspirin), dll kompensasi adalah terkait
pernapasan

Metabolic Alkalosis:
 Disebabkan oleh peningkatan pH (> 7,45) terkait
dengan kelebihan dalam plasma HCO3-
 Disebabkan oleh hilangnya ion H +, laba
bersih dalam HCO3-, atau hilangnya Cl-ion
yang melebihi HCO3-
 Kebanyakan HCO3-berasal dari CO2 yang
dihasilkan selama proses metabolisme,
reabsorpsi HCO3 disaring-, atau generasi
baru HCO3-oleh ginjal
 Proal tubulus diserap 99,9% disaring
HCO3-; kelebihan diekskresikan dalam urin

Alkalosis metabolik manifestasi:

 Tanda & gejala (s/SX) penipisan volume atau

hipokalemia
 Hypoventilory kompensasi, Hipoksemia
& pernafasan asidosis
 Neurologis s/SX mungkin termasuk
kebingungan mental, refleks hiperaktif,
tetani dan spasme carpopedal
 Alkalosis parah (> 7,55) menyebabkan
kegagalan pernafasan, dysrhthmias,
kejang & koma

Pengobatan alkalosis metabolik:

 Koreksi penyebab ketidakseimbangan

 Mei termasuk suplementasi KCl untuk K
+/Cl-defisit
 Penggantian cairan dengan 0,9 normal
saline atau 0,45 normal saline untuk
s/SX penipisan volume
 Intubasi & ventilasi mekanis mungkin
diperlukan jika terjadi kegagalan
pernafasan

Metabolic Acidosis:
 Defisit primer pada basis HCO3-(< 22 mEq/L)
dan pH (< 7,35)
 Disebabkan oleh 1 dari 4 mekanisme
 Peningkatan asam metabolik nonvolatil,
penurunan sekresi asam oleh ginjal,
hilangnya berlebihan HCO3-, atau
peningkatan Cl-
 Meningkatkan asam metabolik
w/akumulasi asam laktat, produksi
berlebih dari ketoacids, atau
obat/konsumsi anion kimia

Asidosis metabolik manifestasi:

 Hyperventialtion (untuk mengurangi tingkat

CO2), & dyspnea
 Keluhan kelemahan, kelelahan, malaise
umum, atau sakit kepala membosankan
 Mungkin juga memiliki anorekdi, N/V, &
sakit perut
 Jika asidosis berlangsung, pingsan,
koma & LOC mungkin menurun
 Kulit sering hangat & flush terkait
dengan stimulasi simpatik

Pengobatan asidosis metabolik:

 Mengobati kondisi yang pertama

menyebabkan ketidakseimbangan
 NaHCO3 infus untuk HCO3-< 22mEq/L
 Restorasi cairan dan pengobatan
ketidakseimbangan elektrolit
 Pemberian tambahan O2 atau ventilasi
mekanis jika sistem pernapasan mulai
gagal

Cepat metabolik Review:

 Gangguan metabolik menunjukkan

kelebihan/defisit pada HCO3-(<
22mEq/L or > 26mEq/L
 Reabsorpsi disaring HCO3-& generasi
baru HCO3-terjadi pada ginjal
 Sistem pernapasan adalah mekanisme
kompensasi
 SELALU memperlakukan gangguan
utama

Gangguan pernapasan:
 Alkalosis: rendah PaCO2 (< 35 mmHg)
 Disebabkan oleh hiperventilasi etiologi
apapun (hipoxemia, kecemasan, PE, edema
paru, kehamilan, ventilasi yang berlebihan
w/ventilator mekanik, dll.)
 Asidosis: ditinggikan PaCO2 (> 45 mmHg)
 Disebabkan oleh Hipoventilasi etiologi
apapun (Sleep Apnea, oversedation, trauma
kepala, overdosis obat, pneumothorax, dll)
 Kompensasi adalah terkait metabolik

Respiratory Alkalosis:
 Ditandai dengan penurunan awal dalam
plasma PaCO2 (< 35 mmHg) atau
hipokapnia
 Menghasilkan elevasi pH (> 7,45)
w/penurunan berikutnya dalam HCO3-(<
22 mEq/L)
 Disebabkan oleh hiperventilasi atau RR
yang melebihi apa yang diperlukan untuk
mempertahankan tingkat PaCO2 normal

Respiratory Alkalosis
Manifestations:
 S/sx are associated w/ hyperexcitiability
of the nervous system & decreases in
cerebral blood flow
 Increases protein binding of EC Ca+,
reducing ionized Ca+ levels causing
neuromuscular excitability
 Lightheadedness, dizziness, tingling,
numbness of fingers & toes, dyspnea, air
hunger, palpitations & panic may result
Treatment of Respiratory
Alkalosis:
 Always treat the underlying/initial
cause
 Supplemental O2 or mechanical
ventilation may be required
 Pt’s may require reassurance,
rebreathing into a paper bag (for
hyperventilation) during symptomatic
attacks, & attention/treatment of
psychological stresses.
Respiratory Acidosis:
 Occurs w/ impairment in alveolar
ventilation causing increased PaCO2
(>45 mmHg), or hypercapnia, along w/
decreased pH (<7.35)
 Associated w/ rapid rise in arterial
PaCO2 w/ minimal increase in HCO3- &
large decreases in pH
 Causes include decreased respiratory
drive, lung disease, or disorders of CW
/respiratory muscles
Respiratory Acidosis
Manifestations:
 Elevated CO2 levels cause cerebral
vasodilation resulting in HA, blurred
vision, irritability, muscle twitching &
psychological disturbances
 If acidosis is prolonged & severe,
increased CSF pressure & papilledema
may result
 Impaired LOC, lethargy/coma, paralysis
of extremities, warm/flushed skin,
weakness & tachycardia may also result
Treatment of Respiratory
Acidosis:
 Treatment is directed toward
improving ventilation; mechanical
ventilation may be necessary
 Treat the underlying cause
 Drug OD, lung disease, chest
trauma/injury, weakness of respiratory
muscles, airway obstruction, etc.
 Eliminate excess CO2
Quick Respiratory Review:
 Caused by either low or elevated PaCO2
levels (<35 or >45mmHg)
 Watch for HYPOventilation or
HYPERventilation; mechanical
ventilation may be required
 Kidneys will compensate by conserving
HCO3- & H+
 REMEMBER to treat the primary
disturbance/underlying cause of the
imbalance
Compensatory Mechanisms:
 Adjust the pH toward a more normal
level w/ out correcting the underlying
cause
 Respiratory compensation by
increasing/decreasing ventilation is
rapid, but the stimulus is lost as pH
returns toward normal
 Kidney compensation by conservation
of HCO3- & H+ is more efficient, but
takes longer to recruit
Metabolic Compensation:
 Results in pulmonary compensation
beginning rapidly but taking time to
become maximal
 Compensation for Metabolic Alkalosis:
 HYPOventilation (limited by degree of
rise in PaCO2)
 Compensation for Metabolic Acidosis:
 HYPERventilation to decrease PaCO2
Begins in 1-2hrs, maximal in 12-24 hrs
Respiratory Compensation:
 Results in renal compensation which
takes days to become maximal
 Compensation for Respiratory Alkalosis:
 Kidneys excrete HCO3-
 Compensation for Respiratory Acidosis:
 Kidneys excrete more acid
 Kidneys increase HCO3- reabsorption
Gas darah arteri normal (ABG)

 PH arteri: 7,35 – 7,45

 HCO3-: 22-26 mEq/L
 PaCO2:35-45 mmHg
 TCO2:23 – 27 mmol/L
 PaO2:80-100 mmHg
 SaO2:95% atau lebih (sapi denyut)
 Kelebihan dasar:-2 hingga + 2
 Anion Gap: 7 – 14

PH asam-basa dan HCO3-

 PH arteri ECF adalah 7,40

 Acidemia: pH darah < 7,35 (peningkatan
H +)
 Alkalemia: pH darah > 7,45 (penurunan
H +) jika HCO3-level adalah gangguan
utama, masalahnya adalah metabolik

 Asidosis: hilangnya asam nonvolatile &
gain dari HCO3-
 Alkalosis: kelebihan H + (ginjal tidak
dapat diekskresikan) & HCO3-rugi
melebihi kapasitas ginjal untuk
meregenerasi

Acid-Base PCO2, TCO2 & PO2
 Jika PCO2 adalah gangguan utama, masalahnya adalah
pernapasan; itu adalah refleksi dari ventilasi alveolar
(paru)
 PCO2 meningkatkan: hipoventilasi hadir
 PCO2 mengurangi: hiperventilasi hadir
 TCO2 mengacu pada Total kandungan CO2
dalam darah, termasuk CO2 yang ada di
HCO3-
 > 70% CO2 dalam darah adalah dalam bentuk
HCO3-
 PO2 juga penting dalam menilai fungsi
pernapasan

Base Excess or Deficit:
 Measures the level of all buffering
systems in the body – hemoglobin,
protein, phosphate & HCO3-
 The amount of fixed acid or base that
must be added to a blood sample to
reach a pH of 7.40
 It’s a measurement of HCO3- excess or
deficit
Anion Gap:
 The difference between plasma
concentration of Na+ & the sum of
measured anions (Cl- & HCO3-)
 Representative of the concentration
of unmeasured anions (phosphates,
sulfates, organic acids & proteins)
 Anion gap of urine can also be
measured via the cations Na+ & K+, &
the anion Cl- to give an estimate of
NH4+ excretion
Anion Gap
 The anion gap is increased in conditions
such as lactic acidosis, and that result
from elevated levels of metabolic acids
(metabolic acidosis)
 A low anion gap occurs in conditions
that cause a fall in unmeasured anions
(primarily albumin) OR a rise in
unmeasured cations
 A rise in unmeasured cations is seen in
hyperkalemia, hypercalcemia, hyper-mag
nesemia
, lithium intoxication or multiple
myeloma
Sodium Chloride-Bicarbonate
Exchange System and pH:
 The reabsorption of Na+ by the kidneys
requires an accompanying anion
- 2 major anions in ECF are Cl- and HCO3-
 One way the kidneys regulate pH of ECF is
by conserving or eliminating HCO3- ions in
which a shuffle of anions is often necessary
 Cl- is the most abundant in the ECF & can
substitute for HCO3- when such a shift is
needed.
Acid-Base w/o Compensation:
Parameters: pH PaCO2 HCO3-
Metabolic Normal
Alkalosis
Metabolic Normal
Acidosis
Respiratory Normal
Alkalosis
Respiratory Normal
Acidosis
 Interpretation Practice:
 pH: 7.31 Right!
Resp. Acidosis

 PaCO2: 48 TryResp.
Again
Alkalosis

 HCO3-: 24 Try Again

Metabolic Acidosis

Resp. Alkalosis
 pH: 7.47 Try Again
Metabolic Alkalosis
 PaCO2 : 45 Right!
Metabolic Acidosis
 HCO3 : 33
-
Try Again

Back to Key
 Interpretation Practice:

 pH: 7.20 Try Again

Metabolic Alkalosis

 PaCO2: 36 Try Again

Resp. Acidosis

 HCO3-: 14 Right!
Metabolic Acidosis

 pH: 7.50 Try Alkalosis

Metabolic Again
 PaCO2 : 29 Right!
Resp. Alkalosis

Resp. Acidosis
 HCO 3
-
-: 22 Try Again

Back to Key
Acid-Base Fully Compensated:
Parameters: pH PaCO2 HCO3-
Metabolic Normal
Alkalosis >7.40
Metabolic Normal
Acidosis <7.40
Respiratory Normal
Alkalosis >7.40
Respiratory Normal
Acidosis <7.40
 Interpretation Practice:
 pH: 7.36 TryResp.
Compensated Again
Alkalosis

 PaCO2: 56 Try Again

Compensated Metabolic Acidosis

 HCO3-: 31.4 Right!

Compensated Resp. Acidosis

Compensated Resp. Alkalosis

 pH: 7.43 Right!
Compensated Metabolic Alkalosis
 PaCO2 : 32 Try Again
Compensated Metabolic Acidosis
 HCO3: 21 Try Again

Back to Key
Acid-Base Partially Compensated:

Parameters: pH PaCO2 HCO3-

Metabolic
Alkalosis
Metabolic
Acidosis
Respiratory
Alkalosis
Respiratory
Acidosis
 Interpretation Practice:

 pH: 7.47 Right!

Partially Compensated Metabolic Alkalosis

 PaCO2: 49 Try Compensated

Partially Again Resp. Alkalosis

Partially Compensated Metabolic Acidosis

 HCO3-: 33.1 Try Again

Partially Compensated Metabolic Alkalosis

 pH: 7.33 Try Again
Partially Compensated Resp. Acidosis
 PaCO2 : 31 Try Again
Partially Compensated Metabolic Acidosis
 HCO3- : 16 Right!

Back to Key
REFERENCES:
 Emily Phillips MSN 621 Spring 2009
 E-mail: emmalemmaRN@hotmail.com All images imported from
 Microsoft Clipart & Yahoo Image gallery

http://www.healthline.com/galecontent/acid-base-balance?
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3/5/09.

Porth, C.M. (2005). Pathophysiology Concepts of Altered Health States (7th

ed.). Philadelphia: Lippincott Williams & Wilkins.

http://en.wikipedia.org/wiki/Dissociation_(chemistry). Retrieved 3/6/09.

http://www.clt.astate.edu/mgilmore/pathophysiology/Acid and Base.ppt#1.

Retrieved 3/6/09.
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http://www.uhmc.sunysb.edu/internalmed/nephro/webpages/Part_E.htm.
Retrieved 3/6/09.

http://medical-dictionary.thefreedictionary.com/Volatile+acid. Retrieved 3/6/09.

http://wiki.answers.com/Q/
How_does_the_phosphate_buffer_system_help_in_maintaining_the_ph_of_
our_body. Retrieved 3/10/09.

Alspach, J.G. (1998). American Association of Critical-Care Nurses Core

Curriculum for Critical Care Nursing (5th ed.). Philadelphia: Saunders.

http://medical-dictionary.thefreedictionary.com. Retrieved 4/14/09.

Acid-Base Balance & Oxygenation Power Point. (2007). Milwaukee: Froedtert

Lutheran Memorial Hospital Critical Care Class.