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Acid Base

Disorders
Wiwi J
Lab / SMF Anestesi & Reaminasi
FK Unibraw / RSU dr Saiful Anwar
Acid Base Disorders
Disorders Primary Compensatory
Charge Response
Respiratory
Acidosis PaCO2 HCO3-
Alkalosis Pa CO2 HCO3-
Metabolic
Acidosis HCO3- Pa CO2
Alkalosis HCO3- PaCO2
Etiology and Treatment of
Respiratory Acidosis
Acidosis
Physiologic Effect of Acidosis
1. Reduced Cardiac Contractility
2. Reduced Peripheral Vascular
Resistance
3. Decreased the threshold for ventricular
fibrillation
4. CNS Depression
5. Hyperkalemia
Etiology of Respiratory Acidosis
1. Alveolar Hypoventilation
1. CNS Depression
Drug Induced
Cerebral Ischemic
Cerebral Trauma
2. Chest Wall Abnormalities
Flail Chest
Kyphoscoliosis
3. Pleural Abnormalities
Pneumothorax
Pleural Effusion
Etiology of Respiratory Acidosis
1. Alveolar Hypoventilation
4. Airway Obstruction
Severe Asthma
COPD
Laryngospasme
5. Parenchymal Lung Disease
Pulmonary Edema
Pneumonia
Aspiration
Pulmonary Emboli
6. Ventilation Malfunction
Etiology of Respiratory Acidosis

2. Increased CO2 Production

Malignant Hyperthermia
Intensive Shivering
Prolonged Seizure Activity
Thyroid Storm
Extensive Thermal Injury
(burns)
Treatment of Respiratory Acidosis
1. Reverse Imbalance between CO2
production and alveolar ventilation
Increasing Alveolar Ventilation
Severe Asthma Bronchodilator
Overdose Narcotics Antidotes
ALO (mild) Diuretics
Reducing CO2 Production
Malignant Hyperthermia Dantrolen
Thyroid Storm Antithyroid
When bicarbonat is needed?
Intravenous NaHCO3 is rarely
necessary unless
pH < 7,10 and HCO3- < 15 mEq/lt

NaHCO3 treatment will transiently


increased PaCO2 because
H+ + HCO3- CO2 + H2O
Etiology and Treatment of
Metabolic Acidosis
Metabolic Acidosis
Mechanism of Pathologic Process
1. Consumption of HCO3- by a strong
nonvolatile acid
2. Renal / GI wasting of HCO3-
3. Rapid dilution of Extra Cellular
Fluid with bicarbonate free fluid
Etiology of Metabolic Acidosis
1. Increased anion gap
1. Increased production of endogenous
nonvolatile acid
Renal failure
Ketoacidosis
Diabetics
Starvation
Lactic acidosis
Mixed
Nonketotic hyperosmolar coma
2. Ingestion of toxin
Salycylate
Methanol
3. Rhabdomyolisis
Etiology of Metabolic Acidosis
2. Normal anion gap ( hyperchloremic)
1. Increased GI losses of HCO3-
Diarrhea
Fistulae (pancreatic, billiary)
2. Increased renal losses of HCO3-
Renal tubular acidosis
CA inhibitor
3. Dilutional
Large amount of bicarbonat
Free fluids (Normal Saline)
4. Total Parenteral Nutrition
5. Increased intake of chloride
Ammonium chloride
Lysine hydrochloride
Anion Gap
Anion Gap =
The diferrence between
the major measured cations &
the major measured anions
Anion Gap =
Major plasma cations Major plasma anions
Anion Gap = (Na+) {(Cl)-+(HCO3)-}
Anion Gap = 140- (104+24)
12 mEq/lt
(Normal range = 7 14 mEq/lt)
Anion Gap
Anion Gap =
unmeasured anions unmeasured cations
Unmeasured anions consist of :
K+, Ca2+ and Mg2+
Unmeasured cations consist of :
All organics anions (include plasma
protein)
Sulfates
Phosphates
Treatment Of Metabolic Acidosis
1. Treat the Etiologic Factor
Diabetic Ketoacidosis
Replace the existing fluid deficit
Restore adequate oxygenation
Restore tissue perfusion
Insulin
2. Administer the bicarbonate if
pH < 7,1
Etiology and Treatment of
Respiratory Alkalosis
Alkalosis
Physiologic Effect of Alkalosis
1. Hb more difficult to give up oxygen to
the tissue
2. Decrease Cerebral Blood Flow
3. Increase systemic vascular resistance
4. Increase bronchial smooth muscle tone
5. Decrease pulmonary vascular
resistance
6. May precipitate coronary vasospasm
Etiology of Respiratory Alkalosis
1. Central Stimulation
1. Pain
2. Fever
3. Infection
4. Stroke
5. Drug Induced
Salicylate
Progesterone (pregnancy)
6. Anxiety
Etiology of Respiratory Alkalosis
2. Peripheral Stimulation
1. Hypoxemia
2. High Altitude
3. Pulmonary disease
Congestive Heart Failure
Noncardiogenic pulmonary edema
Asthma bronchial
4. Severe Anemia
Etiology of Respiratory Alkalosis
3. Unknown Mechanism
1. Sepsis
2. Metabolic encephalopathies
4. Iatrogenic
Ventilator Induced
Treatment of Respiratory Alkalosis
1. Correction of the underlying
disease / process
2. For severe alkalemia (pH>7.60)
1. Amonium Chloride (0,1mol/lt)
2. Arginine hydrocloride
Etiology and Treatment of
Metabolic Alkalosis
Etiology of Metabolic Alkalosis
1. Chloride Sensitive
1. Gastrointestinal
Vomiting
Diarrhea
Gastric drainage
2. Renal
Diuretics
Low chloride intake
3. Sweat
Cystic fibrosis
Etiology of Metabolic Alkalosis
2. Chloride Resistance
1. Increased mineralocorticoid
activity
Primary hyperaldosteronism
Secondary hyperaldosteronism
(edematous disorders)
Cushings syndrome
2. Severe hypokalemia
Etiology of Metabolic Alkalosis
3. Miscellaneous
1. Massive blood transfusion
2. Acetate containing colloid
solutions
3. Alkaline administration with renal
insufficiency
Alkali therapy
4. Hypocalcaemia
Bone metastases
5. Glucose feeding after starvation
Treatment of Metabolic Alkalosis
1. Treat the underlying disease
Excessive loss of gastric fluid
H2 Blocker
Primary hyperaldosteronism
Aldosterone antagonist
(spironolactone)
Chloride sensitive metabolic
alkalosis (eg: long diuretic
treatment)
NaCl administration &
KCl replacement
Treatment of Metabolic Alkalosis
2. If pH > 7.6 =
Ammonium Chloride (0,1 mol/lt)
Vitamin C (5-10 g/day)
Hemodyalisis
Balanced Solution

Contains of stable anions (lactate,


gluconas and acetate)

Available here in crystalloid and colloid


solution
Thank You
Matur Sembahnuwun