Professional Documents
Culture Documents
Dr Amith Sreedharan
DISCUSSION HEADINGS
• BASICS
• NORMAL PHYSIOLOGY
• ABNORMALITIES
• METABOLIC ACID BASE DISORDERS
• RESPIRATORY ACID BASE DISORDERS
• ALTERNATIVE CONCEPTS
• Acid
Any compound which forms H⁺ ions in
solution (proton donors)
eg: Carbonic acid releases H⁺ ions
• Base
Any compound which combines with
H⁺ ions in solution (proton acceptors)
eg:Bicarbonate(HCO3⁻) accepts H+ ions
Acid–Base Balance
Normal pH : 7.35-7.45
Acidosis
Physiological state resulting from abnormally low plasma pH
Alkalosis
Physiological state resulting from abnormally high plasma pH
• pH = 6.1 + log([HCO3-]/.03xpCO2)
1.Buffering
2. Compensation
Buffers
First line of defence (> 50 – 100 mEq/day)
Two most common chemical buffer groups
– Bicarbonate
– Non bicarbonate (Hb,protein,phosphate)
Blood buffer systems act instantaneously
Regulate pH by binding or releasing H⁺
Carbonic Acid–Bicarbonate Buffer System
Carbon Dioxide
Most body cells constantly generate carbon dioxide
Most carbon dioxide is converted to carbonic acid, which dissociates
into H+ and a bicarbonate ion
Metabolic Alkalosis
Metabolic Alkalosis
Decreased myocardial contractility
Arrythmias
• Hypoventilation
pulmonary micro atelectasis
V/Q mismatch(alkalosis inhibits HPV)
Contraction Alkalosis
• Loss of HCO₃⁻ poor, chloride rich ECF
• Contraction of ECF volume
• Original HCO₃⁻ dissolved in smaller volume
• ↑HCO₃⁻ concentration
• Eg : Loop diuretics/Thiazides in a generalised
edematous pt.
Respiratory Acidosis
• ↑ PCO₂ → ↓pH
• Acute(< 24 hours)
• Chronic(>24 hours)
RESPIRATORY ACIDOSIS - CAUSES
CNS DEPRESSION
DRUGS:Opiates,sedatives,anaesthetics
OBESITY HYPOVENTILATION SYNDROME
STROKE
NEUROMUSCULAR DISORDERS
NEUROLOGIC:MS,POLIO,GBS,TETANUS,BOTULISM,
HIGH CORD LESIONS
END PLATE:MG,OP POISONING,AG TOXICITY
MUSCLE:↓K⁺,↓PO₄,MUSCULAR DYSTROPHY
AIRWAY OBSTRUCTION
COPD,ACUTE ASPIRATION,LARYNGOSPASM
CONT..
CHEST WALL RESTRICTION
PLEURAL: Effusions,
empyema,pneumothorax,fibrothorax
CHEST WALL: Kyphoscoliosis, scleroderma,ankylosing
spondylitis,obesity
SEVERE PULMONARY RESTRICTIVE DISORDERS
PULMONARY FIBROSIS
PARENCHYMAL INFILTRATION: Pneumonia, edema
ABNORMAL BLOOD CO₂ TRANSPORT
DECREASED PERFUSION: HF,cardiac arrest,PE
SEVERE ANEMIA
ACETAZOLAMIDE-CA Inhibition
RED CELL ANION EXCHANGE: Loop diuretics, salicylates,
NSAID
Compensation in Respiratory Acidosis
Acute resp.acidosis:
Mainly due to intracellular buffering(Hb,Pr,PO₄)
HCO₃⁻ ↑ = 1mmol for every 10 mmHg ↑ PCO₂
Minimal increase in HCO₃⁻
pH change = 0.008 x (40 - PaCO₂)
Chronic resp.acidosis
Renal compensation (acidification of urine &
bicarbonate retention) comes into action
HCO₃⁻ ↑= 3.5 mmol for every 10 mm Hg ↑PCO₂
pH change = 0.003 x (40 - PaCO₂)
Maximal response : 3 - 4 days
Acid–Base Balance Disturbances
Chronic resp.alkalosis:
Renal compensation (acid retention,HCO₃⁻ loss)
Starts after 6 hours, maximal response 2- 3 days
Magnitude : 5mmol/L ↓HCO₃⁻ for 10mmHg ↓PCO₂
LIMIT: 12-15 mmol/L HCO₃⁻
Acid–Base Balance Disturbances