This lecture explains the basics of acid base disorders.
Outline of Lecture
Acid – Base Disorders
what is pH ?
-log [H+]
log 1/[H+]
Blood pH
Sources of Hydrogen Ions
Most hydrogen ions originate from cellular metabolism
Breakdown of phosphorus-containing proteins releases phosphoric acid into the ECF
Anaerobic respiration of glucose produces lactic acid
Fat metabolism yields organic acids and ketone bodies
Transporting carbon dioxide as bicarbonate releases hydrogen ions
Acid-Base Homeostasis
DEFENCE AGAINST pH CHANGE BUFFERS
Proteins
Haemoglobin
Phosphate
Bicarbonate
Bone buffers
Protein Buffer System
Plasma and intracellular proteins are the body’s most plentiful and powerful buffers
Some amino acids of proteins have:
Free organic acid groups (weak acids)
Groups that act as weak bases (e.g., amino groups)
BICARBONATE BUFFER SYSTEM
Henderson-Hasselbalch Equation
CO2 + H2O H2CO3 H + HCO3-
pH = pK + log [Base] / [Acid]
7.4 = 6.1 + log [HCO3–] / [H2 CO3]
7.4 = 6.1 + log 1.3
= 6.1 + [20/1]
Reabsorption of Bicarbonate
Phosphate Buffer System
Nearly identical to the bicarbonate system
Its components are:
Sodium salts of dihydrogen phosphate (H2PO4¯), a weak acid
Monohydrogen phosphate (HPO42¯), a weak base
This system is an effective buffer in urine and intracellular fluid
Hydrogen Ion Excretion
Ammonium Ion Excretion
Pulmonary function
Acid-Base in the G-I Tract
NORMAL
Acid-Base Disorders
METABOLIC ACIDOSIS
Metabolic acidosis
Metabolic acidosis
Increased H+ formation
Acid ingestion
Reduced renal H+ excretion
Loss of bicarbonate
Increased H+ formation
ketoacidosis, diabetic or alcoholic
lactic acidosis
poisoning
inherited organic acidoses
Reduced H+ excretion
Diabetic keto-acidosis
Lactic acidosis
METABOLIC ALKALOSIS
The primary lesion in metabolic alkalosis is increased [HCO3–] from 25®40 mmol/L
The compensatory response to elevated plasma bicarbonate is increased PCO2 from 4050 mmHg
Observe pH from 7.67.5
Metabolic Alkalosis
RESPIRATORY ACIDOSIS
Respiratory Acidosis
This is a disorder of ventilation.
Rate of CO2 elimination is lower than the production
Main categories:
CNS depression
Cardiac arrest
Air way obstruction
Pleural disease
Lung diseases such as COPD and ARDS
Musculoskeletal disorders
Compensatory mechanism for metabolic alkalosis
RESPIRATORY ALKALOSIS
Respiratory Alkalosis
CO2 reduction due to excessive ventilation :
CNS : anxiety, hypoxia, head trauma, infection, fever
Pulmonary: PE , Pneumonia, RDS, high altitude, mild edema
Metabolic : Pregnancy ,Gram negative sepsis
MIXED ACIDOSIS
Laboratory investigations
Biochemical diagnosis
pH
HCO3–
PCO2
Base excess
Etiological diagnosis
Chloride and anion gap
Electrolytes
Urea/creatinine
Glucose
Ketones
Lactate
Urinary chloride
Sequential Rules:
Rule #1
Must know the pH; pH determines whether the primary disorder is an acidosis or an alkalosis
Rule #2
Must know the PaCO2 and serum HCO3–
Rule #3
Must be able to establish that the available data (pH, PaCO2, and HCO3–) are consistent
Acid-Base :Summary
Acid Base Disturbances
Be sure abnormalities not due to lab error
Henderson-Hasselbach equation
[H+] =24 x (pCO2/HCO3)Convert [H+] to pH:
Subtract calculated [H+] from 80; this gives the last two digits of a pH beginning with 7
example: calculated [H+] of 24 converts to pH of (80-24)~7.56
example: calculated [H+] of 53 converts to pH of (80-53)~7.27
Refer to table 1 in handout for more precise conversion, or if calculated [H+] exceeds 80