KESEIMBANGAN

ASAM-BASA (2)
Sudarno, dr M.Kes.
 Gangguan Keseimbangan asam-basa
 Umumnya disertai perubahan kadar elektrolit
dalam plasma
 H+ tak dapat menumpuk tanpa anion yang
menyertainya (misalnya Cl-, SO42- , laktat-)
atau tanpa pertukaran dengan kation
(misalnya Na+, K+)
 Jadi pengukuran keadaan keseimbangan asam
basa perlu pemeriksaan:
 pH darah
 pCO2 darah
 Kadar elektrolit darah : Na+, K+, Cl-
 dll
 Acid-Base Imbalances
 pH< 7.35 acidosis
 pH > 7.45 alkalosis
 The body response to acid-base imbalance is
called compensation
 May be complete if brought back within
normal limits
 Partial compensation if range is still outside
norms.
 Primary Acid-Base Disorders
As dictated by the Henderson-Hasselbalch equation,
disturbances in either the respiratory component (pCO2) or
metabolic component (HCO3-) can lead to alterations in pH.

Metabolic Acidosis Metabolic Alkalosis

(Too little HCO3-) (Too much HCO3-)

Respiratory Acidosis Respiratory Alkalosis

(Too much CO2) (Too little CO2)
 Compensation
When a primary acid-base disorder exists, the body
attempts to return the pH to normal via the “other
half” of acid base metabolism.

Primary metabolic disorder  Respiratory compensation

Primary respiratory disorder  Metabolic compensation

 Compensation
 If underlying problem is metabolic,
hyperventilation or hypoventilation can help :
respiratory compensation.
 If problem is respiratory, renal mechanisms
can bring about metabolic compensation.
 Acidosis
 Principal effect of acidosis is depression of the
CNS through ↓ in synaptic transmission.
 Generalized weakness
 Deranged CNS function the greatest threat
 Severe acidosis causes
 Disorientation

 coma

 death
 Alkalosis
 Alkalosis causes over excitability of the central and
peripheral nervous systems.
 Numbness
 Lightheadedness
 It can cause :
 Nervousness

 muscle spasms or tetany

 Convulsions

 Loss of consciousness

 Death
 Compensation (continued)
Primary Disorder Compensatory Mechanism
Metabolic acidosis Increased ventilation

Metabolic alkalosis Decreased ventilation

Respiratory acidosis Increased renal reabsorption of HCO3-

in the proximal tubule
Increased renal excretion of H in the
distal tubule
Respiratory alkalosis Decreased renal reabsorption of HCO3-
in the proximal tubule
Decreased renal excretion of H+ in the
distal tubule
 The Arterial Blood Gas (ABG)

pH, pCO2, pO2 – Measured directly

HCO3-, O2 saturation (usually) – Calculated from pH, pCO2, and pO2

 Practical Approach

* Check the pH

If the pH < 7.35, acidemia (and at least 1 acidosis) is present.

If the pH > 7.45, alkalemia (and at least 1 alkalosis) is present.

 Practical Approach
* Check the pCO2

pH < 7.35 and pCO2 < 40  metabolic acidosis

pH < 7.35 and pCO2 > 40  respiratory acidosis

pH > 7.45 and pCO2 < 40  respiratory alkalosis

pH > 7.45 and pCO2 > 40  metabolic alkalosis
 Practical Approach

* Calculate the anion gap

Anion gap = [Na+ + K + ) – ( [Cl-] + [HCO3-] )

If the anion gap is elevated, an elevated gap metabolic acidosis

is likely present.

 Clinicians use the anion gap to identify the cause of metabolic acidosis.
 Anion Gap
 Normal = 12 + 2

Na+ Cl-

K+
= Albumin

HCO3-
Other Cations Other Anions
Phosphate, sulphate, organic anions

(Na+ + K+ ) - (Cl- +HCO3-) = Anion Gap

 Anion Gap in Metabolic Acidosis
 Salicylates raise the gap to 20.
 Renal failure raises gap to 25.
 Diabetic ketoacidosis raises the gap to 35-40.
 Lactic acidosis raises the gap to > 35 (>50).
 Largest gaps are caused by ketoacidosis and
lactic acidosis.
 Metabolic acidosis – normal
anion gap

Bicarbonate loss
 – GI loss

 – Renal tubular acidosis

 – Renal failure

Chloride is retained so anion gap is normal

 Metabolic acidosis – raised anion
gap
Addition of unmeasured anions

 Ketoacidosis
– Diabetes
 Lactic acidosis
– Tissue hypoxia (Type A)
– Drugs eg phenformin, ethanol, methanol
(Type B)
 Practical Approach

* If an elevated gap acidosis is present, calculate the

delta-delta ratio, to determine if a second metabolic
disorder is present.

Delta–Delta = Measured anion gap – Normal anion gap

Normal [HCO3-] – Measured [HCO3-]
 Practical Approach

* If a metabolic acidosis is present, check the urine

pH.

Urine pH > 6.0 in the setting of an acidosis  Suggests RTA

 Practical Approach

8. Generate a differential diagnosis

If multiple disorders are present, they may be:

All related to the same process

All independent of one another
 Asidosis Metabolik
 Primer kekurangan bikarbonat (HCO3-) < 22 meq/L
 Asidosis : pH  konsentrasi H+
[HCO3-]
 Sebab; [H2CO3]

 Produksi asam organik > laju eliminasinya

 Misalnya pembentukan senyawa keton pada
asidosis diabetik Diabetic ketoacidosis raises
the gap to 35-40
 ekskresi asam
 Misalnya gagal ginjal, asidosis tubular
 Kehilangan HCO3- berlebihan
 Misalnya diare hebat  kehilangan cairan
duodenal
 Symptoms of Metabolic Acidosis
 Headache, lethargy
 Nausea, vomiting, diarrhea
 Coma
 Death
 Compensation for Metabolic
Acidosis
 Increased ventilation
 Renal excretion of hydrogen ions if possible
 K+ exchanges with excess H+ in ECF
 ( H+ into cells, K+ out of cells)
 As H+ ions start to accumulate,

chemical buffers (plasma bicarbonate & proteins)

in the cells and extracellular fluid bind with them
in attempt to buffer the acid (H+).

At this early stage, the patient may be

asymptomatic.
 Excess H+ ions, that aren’t bound to the buffers,
decrease the pH and stimulate the chemoreceptor in
the brain’s medulla.

 This triggers an increase in the respiratory rate

resulting in an increase in CO2. (HIPERVENTILASI)

 This lowers the PaCO2 allowing more H+ to bind with

the bicarbonate (HCO3-) ions.

 Look for a bicarbonate level < 18 mEq/L, a pH of <

7.35, a falling PaCO2, and tachypn
 If the kidneys are healthy and mature,
they will compensate for the continuing acidosis by
secreting excess H+ ions into the renal tubules.

Once in the tubules, the H+ ions are buffered by

phosphate or ammonia and excreted into the urine in
the form of a weak acid.

Look for a more acidic urine.

 Each time a H+ ion is secreted into the renal tubule,

a sodium (Na+) and bicarbonate ion are absorbed from

the tubule into the circulating blood volume.

Look for a slow return of the bicarbonate level and pH. to

normal
 Bila kompensasi berjalan sempurna dikatakan
asidosis metabolik terkompensasi sempurna
 Bila dengan kompensasi pH tetap <7,35
dikatakan terkompensasi sebagian

 Mekanisme kompensasi:
 Bufer kimia: terutama oleh bufer
bikarbonat/asam karbonat
 Bufer fisiologis(pernafasan): pH yang
turun merangsang Hiperventilasi agar
ekskresi CO2 meningkat  [H2CO3] 
agar ratio [HCO3-]/[H2CO3] kembali
20/1
 Bufer fisiologis (renal)
 Ginjal berusaha mengembalikan
komposisi elektrolit semula dan PH
dengan cara ekskresi asam dan
menahan basa
 pertukaran Na+-H+
 pembentukan ammonia
 reabsorpsi HCO3-
 IV lactate solution
Treatment of Metabolic Acidosi
 Metabolic acidosis

H+ + HCO3 H2CO3 CO2 + H2O

Compensation by
Blowing off CO2
 Asidosis Respiratorik

Primer [H2CO3]: primary event berlebihan

CO2 >45 mmHg
 pH
 Respiratory Acidosis
 Hypercapnia – high levels of CO2 in blood
 Chronic conditions:
 Depression of respiratory center in brain that controls
breathing rate – drugs (morphin) or head trauma
 Paralysis of respiratory or chest muscles
 Emphysema bronchopneumoni, status asthmaticus
bronchiale, fibrosis paru2
* Acute conditons:
Adult Respiratory Distress Syndrome
Pulmonary edema
Pneumothorax
Signs and Symptoms of Respiratory
Acidosis
 Breathlessness
 Restlessness
 Lethargy and disorientation
 Tremors, convulsions, coma
 Respiratory rate rapid, then gradually
depressed
 Skin warm and flushed due to vasodilation
caused by excess CO2
 [HCO3-]
[H2CO3]

Pulmonary ventilation decreases,

CO2 levels increase and combine with water

(H2O) to form carbonic acid (H2CO3) in larger
than normal amounts.

The excessive carbonic acid causes the drop in

the pH. The carbonic acid dissociates (breaks
apart) to release free H+ ions and bicarbonate
ions (HCO3).
Look for a PaCO2 level >45 mm Hg and a pH of < 7.35.
 HIPERVENTILASI

As PaCO2 levels continue increasing,

CO2 accumulates in the body tissues and fluids, including
cerebrospinal fluid and the respiratory center in the
medulla.
Like in the blood, the CO2 combines with H2O to form
H2CO3, which in turn dissociates into H+ and HCO3- ions.
This increase in CO2 and H+ ions stimulates the respiratory
center to increase the respiratory rate (correction) to
excrete the excess CO2 and bring the pH back into normal
range. If correction is successful:
Look for increased respiratory rates, perhaps shallow
respirations, a decreasing PaCO2 and an increasing pH.
 Compensation for Respiratory
Acidosis
 Kidneys eliminate hydrogen ion and retain
bicarbonate ion
 Mekanisme kompensasi:
 Bufer biologis: Asam karbonat yang
masuk dalam darah yang berlebihan
terutama dibufer oleh Hb dan sistem
bufer protein
 Bufer fisologis (paru2): pCO2 yang
meningkat merangsang pusat
pernapasan menaikkan laju pernapasan
(asal kelainan primer bukan pada pusat
pernapasan) 
Pengeluaran CO2 lewat paru
 Bufer fisiologis (renal)
 pertukaran Na+-H+
 pembentukan ammonia
 reabsorpsi HCO3-
 As respiratory mechanisms (correction) fail,
the increasing PaCO2 stimulates the kidneys to retain
both HCO3- and sodium (NA+) ions and to excrete H+
(compensation) ions.

The H+ is excreted as free H+ and some as ammonium

(NH4).

Meanwhile, the NA+ and HCO3- ions combine to form

sodium bicarbonate (NaHCO3),
 Treatment of Respiratory Acidosis
 Restore ventilation
 IV lactate solution
 Treat underlying dysfunction or disease
  Respiratory acidosis

H+ + HCO3 H2CO3 CO2 + H2O

Primary event =
retention of CO2

 Respiratory acidosis - Compensated

H+ + HCO3 H2CO3 CO2 + H2O

Renal retention of
Bicarbonate
minigates level of acidosis
Primary event =
retention of CO2
SELAMAT BELAJAR
 Alkalosis Respiratorik
 Primer kekurangan [H2CO3] pCO2
 pH
 Sebab:
Semua keadaan yang menyebabkan meningkatnya
laju (rate) atau kedalaman (depth) pernapasan,
atau keduanya
Misalnya demam , suhu luar yang tinggi, histeria
yang menyebabkan hiperventilasi, hipoksia, dan
keracunan salisilat

Eliminasi CO2 yang berlebihan menurunkan [H2CO3]

 ratio [HCO3-] / [H2CO3] pH
 Mekanisme kompensasi:
 Terutama dilakukan oleh bufer fisiologi (renal )
 Mekanisme renal
 pertukaran Na+-H+
 pembentukan ammonia
 reabsorpsi HCO3-