Acid base.txt

• Strong base (HCO3-) and conjugate weak acid (H+)
• HB H+ + B-

• Bicarbonate: high capacity and ease of elimination (CO2)
• Phosphate
• Plasma proteins
• Intracellular buffers eg Hb

• Difference between measured and calculated osmolality
• Calculated: 2(Na + K) + urea + glucose

The presence of an osmolar GAP in metabolic acidosis indicates presnce of unmeasured osmoles eg methanol, ethanol, ethylene glycol

• Positively charged
• Sodium Na+

• Negatively charged particles
• Chlrodie Cl-

(Na + K) – (Cl + HCO3)

12-16mmol/l

It will lower the bicarbonate level (think equation)

Amount of acid added

Monitor patients response to therapy

Acid added endogenously or exogenously lower bicarb concentration less anions greater GAP

Loss of bicarbonate associated with HYPERCHLORAEMIA so anion gap remains normal! (as Cl- is an anion)

• Big MUDPILES
• Biguanides: metformin
• Methanol
• Uraemia
• DKA, alcoholic ketoacidosis (B-hydroxybutyrate, acetoacetate, acetone)
• Paraldehye (fixative)
• Isoniazid, iron, infection
• Lactate
• Ethylene glycol
• Salicylates

• HARD UP AA
• Hyperalimentation
• Acetozolamide (carbonic anhydrase inhibitor)
• Renal tubular acidosis
• Diarrhoea
• Ureto-enteric fistula
• Pancreatico-duodenal fisutla
• Addison’s
• Ammonium chloride ingestion

• GI loss of bicarbonate: small bowel secretions in diarrhoea or pancreatic drainage
• Renal tubular acidosis

Hypokalaemic Hyperchloraemic metaboic acidosis with normal anion gap

Inability to excrete H+

Distal tubule

Over 5.5 (ie failure to acidify urine)

• 1. Rickets/osteomalacia due to buffering of H+ with calcium in bone
• 2. nephrocalcinosis with renal calculi leading to recurrent UTI

• Hypercalciuria from bone
• Decreased urinary citrate: as reabsorbed from urine as a buffer for H+
• Alkaline urine
• All favour calcium phosphate stone formation

• 1. Urinary pH > 5.3 in face of systemic acidosis
• 2. failure to acidify urine following an oral acid load challenge: alluminium chloride test

• Sodium bicarbonate or citrate
• correct the acidemia and reverse bone demineralisation.

• Idiopathic
• Autoimmune: Sjogren’s, SLE

Inability to reabsorb bicarbonate (bicarb leak)

Proximal tubule

• Fanconi syndrome
• Tubulointerstitial disease: myeloma
• Drugs: lead

• Hypokalaemic, hyperchloraemic metablic acidosis
• Normal anion gap

• In type 2: tubules are able to reabsorb SOME HCO3
• So urine can acidify during systemic acidosis

Fanconi syndrome (generalised dysfunction of proximal tubule cells)

Type 1

Due to osmotic diuretic effect of reduced HCO3 reab increased flow rate to distal tubule increased K+ excretion

Iv sodium bicarbonate load: if see high fractional excretion (>15%) of HCO3 = type 2 RTA

High doses of bicarbonate (often intolerable)

• Combination of type 1 and 2 RTA
• Very rare

Hyperkalaemic

Hyporeninaemic, hypoaldosteronism

• Low aldosterone causes hyperkalaemia and acidosis
• As it decreases K+ and H+ secretion

• 1. acts on nuclear mineralocorticoid receptors (MR) in distal tubule and collecting duct in kidney to activate Na/K/ATP pump on basolateral membrane of cell. So sodium is reabsorbed into the blood and K+ is secreted into the urine
• 2. upreg EnaC on apical membrane to increase permeability of Na
• 3. Cl- reab with Na to maintain electrochemical balance
• 4. stimulates uptake of K+ into CELLS
• 5. stimulates H+ secretion in collecting duct, regulating HCO3- levels (acid-base)
• 6. acts on posterior pituitary gland to release ADH

• Hypoadrenalism: hypoaldo
• Mild renal impairment: DM or tubulointerstitial disease
• Drugs: K+ sparing diuretics, ACEi, ARB, NSAID

• Remove cause
• Fludrocortisone
• Furosemide
• Calcium resonium to control hyperK+

• Disturbance of proximal tubule function
• So defective reabsorption of amino acids, K+, phosphate, glucose, bicarbonate (leading to type 2 RTA)

• Idiopathic
• Inherited: errors of metabolism eg fructose intolerance, GSD
• Acquired: tubule damage from heavy metal eg lead, mercury
• Light chain damage: myeloma or amyloidosis

• Remove cause
• Replace losses – K+, HCO3-

• Air hunger
• Neuro symptoms coma
• Impaired cardiac function and state of shock
• Severe acidosis: cardiac dysrhythmias, cardiac arrest, sudden death

• Raised: pH & bicarbonate
• Compensated by: rise in CO2

• Loss of H+/retain bicarb
• Vomit,
• Renal loss from hyperaldosteronism (Conn’s/Cushing’s): retention of Na+ but loss of H+ into urine
• Diuretics (thiazide and loop): K+ depletion
• Burns
• Retention of bicarbonate: administration of alkali with decreased GFR
• Posthypercapnic metabolic acidosis (compensatory)

• Orthostatic hypotension
• Hypokalaemia leading to weakness and hyporeflexia
• Tetany
• Neuromuscular excitability: due to reduced free (active) calcium concentration as it is bound to albumin (as H+ is not bound to it)

• Hypoventilation and subsequent rise in PCO2
• CO2 forms carbonic acid = source of H+
• CO2 + H20 H2CO3 HCO3- + H+
• Airway obstruction: laryngospasm/bronchospasm cause ACUTE RA, COPD cause CHRONIC RA
• Respiratory centre depression: sedative overdose, brain lesions
• Neuromuscular disorder: respiratory muscle diseaes, MS
• Restriction defect: respiratory muscle disease, pneumothorax, interstitial fibrosis, kyphoscoliosis

• Peripheral VASODILATION
• Increase ICP
• Confusion
• Myoclonus
• Coma

• (Hyperventilation reduces CO2) SHAPS
• Salicylates: give MIXED acid base too
• Hypoxia: Congestive cardiac failure, congenital heart disease
Acute asthma (NB if life threatening, may give respiratory acidosis if cant breathe out)
• Psychogenic hyperventilation: fear, anxiety, PAIN
• SAH

lightheaded, parasthesiae, numbness around the mouth, tingling sensation in the hands and feet. Tetany

• Salicylates stimulate resp centre over ventilate and cause resp ALKALOSIS
• Get excess production of lactic acid metabolic ACIDOSIS

The illness accompanying renal failure

• Asterixis
• Tremor
• Hyperreflexia
• Upgoing planter response
• Pericarditis
• Bruising
• Fall in BP and body temp