Acid Base Balance

Ghada Hasab-Allah Abd-Allah

Assisstant Lecturer
Department of Forensic Medicine & Toxicology
Faculty of Medicine - Cairo University
Basic Definitions
 Acid
 Base
 Buffer
 Henderson Hasselbach’s equation
pH & not [H+] Why ?
 [H+] is extremely small
 Measured in nmol/L
 All other cations are measured in mmol/L

 pH which is -log [H+] is more logical

However,
 It moves in the opposite direction
 pH is not linear
• 7.1 7.0 = 80 100
• 7.4 7.3 = 40 50
 pH gives a false impression of biological
sensitivity
• 6.8 7.4 7.8
• 160 40 16
Why [H]+ & [HCO3]- homeostasis?
 Optimize
• Enzyme activity
• Hb saturation with O2
• Myocardial contractility
• Rates of cellular chemical reactions
Regulation of arterial pH
 Buffer systems Most rapid
 Ventilatory responses
 Renal responses Most powerful
Buffer systems
 Bicarbonate 50% Of the total buffering capacity
 Hemoglobin
 Protein
 Phosphate
 CO2 Hydrated to form carbonic
produced acid

Dissociates to H+ &
HCO3-

H is buffered by
HCO3 acts as a buffer
reduced Hb
 Acid base derangement
pH HCO3 PaCO2 Compens.

Acidosis    vent
Metabolic
Alkalosis    vent

Acidosis   
Renal
Respiratory HCO3
Exc
Slight compensation = acute disorder
Alkalosis = chronic
Moderate compensation  
disorder 
 pH
7.36-7.44

Low High
Acidosis Alkalosis
<7.36 >7.44

PaCO2 PaCO 2

High Norm al Low Norm al or high

Respiratory Acidosis HCO 3 Respiratory Alkalosis H CO3

Low High

HCO 3 Meta bolic Acidosis H CO3 Meta bolic Alkalosis

high Low

Trial for com pensation T rial for com pensation

Metabolic acidosis
  [HCO3-] &  pH
 To know the nature of the abnormality
we must identify the anion gap

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

 Normal 12-18 mmol/L

 Metabolic Acidosis

Normal Anion gap High Anion gap

Bicarbonate loss Exogenous acid Overproduction of acid Exogenous acid

Extrarenal Renal HCl, NH4Cl, Arginine or lysine HCl Diabetic ketoacidosis Salicylates
Lactic acidosis Methanol
Starvation ethylene glycol

Diarrhea Renal tubular necrosis

Billiary & Pancreatic Fistula Carbonic anhydrase inhibitors
ileostomy
ureterosigmoidostomy
 Metabolic Acidosis

Normal Anion gap High Anion gap

HCO3 loss Added acids

 production Added acids

Renal Extrarenal
Diabetic Salicylates
RTN Diarrhea ketocidosis
Methanol
CAI Fistulae Lactic acid
Ethylene
ileostomy starvation glycol
Dilutional (hyperchloremic) acidosis
 IV saline fluids at a rate > 30 ml/kg/h
 Dilutes the plasma HCO3 concentration
 Led to introduction of lactated Ringer
solution
Compensatory mechanisms

 Increased alveolar ventilation

 Increased renal secretion of [H]+

 Clinical Manifestation of
Metabolic Acidosis
 Reduced COp
 Pulmonary hypertension
 Arrhythmias
 Kussmaul breathing
 Hyperkalemia
 Treatment
 Identification of the cause
 pH < 7.2 HCO3 < 10 mmol/L
Replace = B.Wt x Base deficit x 0.3
1/2 correction
 Rapid correction

Tetany & convulsions

Remember: hyperventilate as bicarb administration will
add CO2 [180 ml for 1mEq/kg]. This attenuates correction
Forms of HCO3
 Sodium Bicarbonate
8.4% 1 mmol/ml
5% 0.6 mmol/ml
1.4% 0.16 mmol/ml

Isotonic sodium bicarbonate

Cardiac arrest
 Previously,  Recently,
Bicarbonate was Bicarbonate was
essential & was given found to exacerbate
empirical in a dose of acidosis in cases of
1 mmol/kg tissue hypoxia, in
addition to
hypernatremia &
hyperosmolarity.
Metabolic Alkalosis
  [HCO3-] with  pH > 7.45
 Hypoventilation as a compensatory
mechanism is limited & not effective
 It can be classified into
• chloride responsive
• Chloride resistant
Chloride-responsive Chloride-resistant
(Urine Cl- < 20 mmol/L) (Urine Cl- > 20mmol/L)
Loss of acid
vomiting •1ry or 2ry hyperaldosteronism
nasogastric suction •Cushing’s syndrome
gastrocolic fistula •Severe hypokalemia
Cl- depletion •Carbenoxolone
Diarrhea
Diuretic abuse
Excessive Alkali
NaHCO3
Antacid abuse
Chloride-responsive Chloride-resistant
Give Saline TREAT THE CAUSE
Volume expansion
Excreion of HCO3
KCl when required

Acetazolamide in volume
overload
H2 receptor antagonists in
nasogastric suction

In life-threatening metabolic alkalosis --- Dilute HCl in a

central vein to avoid thrombophlebitis
0.1 normal HCl in G5% at a rate < 0.2 mmol/kg/h
Respiratory Acidosis
  PaCO2  pH
 Compensation by  HCO3
 C/P
 HR,  BP, Arrhythmias
 ICP
• COMA
Causes of Respiratory Acidosis
CNS causes PNS causes
Drug overdose Polyneuropathy
Trauma Myasthenia G
Tumour Poliomyelitis
Infection Tetanus
Cerebrovascular Organophosph poisoning

Primary pulmonary disease

- Airway obstruction
- Parenchymal disease
- Loss of mechanical integrity
Treatment of Respiratory Acidosis
 Reverse the underlying cause if possible

 Mechanical ventilation
Respiratory Alkalosis
  PaCO2  pH
 pH > 7.4
 Acute
• Cerebral VC  CBF
• Confusion, Convulsions,
• Circum-oral numbness, tetany
Causes of Respiratory Alkalosis
 Hyperventilation
• Conscious patients during delivery
• Ventilated patients