5. Basics
Definition of acid:
• CICM: A proton donor or H+ ion donor.
• IUPAC: A molecular entity or chemical species capable of donating a hydron (proton)
(see Brønsted acid) or capable of forming a covalent bond with an electron pair (see
Lewis acid).
Definition of base
• CICM: A proton donor or H+ ion donor.
• IUPAC: A chemical species or molecular entity having an available pair of electrons
capable of forming a covalent bond with a hydron (proton) (see Brønsted base) or with
the vacant orbital of some other species (see Lewis base).
6. Buffer
• A solution containing substances that have the ability
to minimise changes in the pH when an acid or base is
added to it.
7. Bicarbonate-carbonic acid buffer pair
• The arterial H+ ion activity can be represented by the
• Henderson equation:
• [H+ ] = 24 x PaCO2 [HCO3 - ]
• Henderson-Hasselbalch equation:
• pH = 6.1 + log [HCO3 - ]/ (PaCO2 x 0.03)
8. • Bicarbonate buffer system in blood
(in vitro) if acid were added at A to
reduce plasma HCO3 - by 50%.
• Stage 1 represents chemical
buffering only,
• Stage 2 represents the added effect
of maintaining pCO2 constant, and
• Stage 3 represents the
compensatory reduction in pCO2
in response to the acid load
9. Haemoglobin Buffer
• Buffering characteristic of haemoglobin is almost
entirely dependent upon the imidazole group of
histidine, which dissociates less when haemoglobin is
in the oxygenated form compared with the
deoxygenated form
• Haemoglobin has twice the concentration of plasma
protein, it has six times the capacity to buffer H+
10. Phosphate Buffer
• pKa of 6.8 and so is a better chemical (or closed) buffer
system than the bicarbonate buffer system.
• In plasma it has one-twentieth the concentration of
bicarbonate, and also operates only as a closed system,
so its capacity is far less than that of the bicarbonate-
carbonic acid buffer.
• In the ICF and in urine, the phosphate buffer system
assumes greater importance.
13. Arterial Blood Gas analysis
• Good clinical practise
• Consider only compressible sites
• Do an Allen’s test prior to obtaining radial-artery
blood sample
• Call for help ( try twice if unsuccessful )
• In Hypotension consider sample from femoral artery
14. Methods of Arterial blood gas
interpretation
• Base deficit method
• Boston method
• Stewart Finkel method
• Physiological method
16. Step 1. Check for validity
• H+ x HCO3- / PaCO2 = 24
• For value of H+
• 80 - ((ph - 7) x 100) for ph between 7.2 and 7.6
• For Ph between 7 and 7.2 add 20 to the result of
above equation
• for Ph 6.9 H+ is 120, 6.8 H+ is 160 and 6.7 its 200
17. Step 2. Change in Ph
• Acidaemia Ph less than 7.35
• Alkalemia Ph more than 7.45
• None Ph between 7.35 and 7.45
18. Step 3 change in PCO2
• Is change in PCO2 contributing to change in Ph or
Reacting to the change in Ph
• Respiratory Acidosis PCO2 > 40
• Respiratory Alkalosis PCO2 < 40
• An acute delta PCO2 change of 10 will change ph
by 0.08
19. Step 4 Change in HCO3
• Is change in HCO3 contributing to change in Ph or
Reacting to the change in Ph
• Metabolic Acidosis HCO3 < 24
• Metabolic Alkalosis HCO3 > 24
• An acute delta change of HCO3 by 10 will change
Ph by 0.15
20. Step 5 Calculate Compensation
• For metabolic acidosis expected PCO2 is
1.5 x HCO3 + 8 with a correction factor of 2
• For metabolic Alkalosis expected PCO2 is
40 + 0.6 (delta HCO3) or 20 + 0.7 HCO3 with a
correction factor of 5
21. Contd...
• For respiratory acidosis
• Acute - a delta change of 10 in PCO2 increase HCO3
by 1 with a correction factor of 3
• Chronic - a delta change of 10 in PCO2 increase HCO3
by 4
• For respiratory alkalosis
• Acute - a delta change of 10 in PCO2 decrease HCO3
by 2
• Chronic - a delta change of 10 in PCO2 decrease
HCO3 by 5
22. Step 6 calculate Anion gap if there is a
metabolic insult
• Anion gap is Na+ - (Cl- + HCO3- ) = 12
• Corrected anion gap = calculated AG + (0.25 (4 -
Albumin in gm/dl)
• AG > 12 implies high anion gap
23. Step 7. If AG is high calculate delta
ratio or delta gap
• Delta ratio is delta AG/ delta HCO3
• Delta Gap is Na - Cl - 36 ( delta AG - delta HCO3)
24. Contd...
• Delta ratio interpretation
• < 0.4 NAGMA
• 0.4 - 0.8 mixed NAGMA plus HAGMA
• 0.8 - 2 pure HAGMA
• > 2 HAGMA with pre existing Metabolic alkalosis
25. Contd...
• Delta Gap Interpretation
• < -6 is mixed NAGMA and HAGMA
• -6 to +6 is Pure HAGMA
• > / = +6 is HAGMA with metabolic alkalosis
26. Step 8 Calculate osmolar gap in
HAGMA or Urinary AG in NAGMA
• Measured osmolarity - calculated Osmolarity
• Calculated Osmolarity is 2 x Na + urea + glucose
• Urinary AG = (Na+) + (K+) - (Cl-)
27. Contd...
• Osmolar gap Interpretation
• Normal < 10
• If high consider presence of Mannitol, toxic
alcohol, Glycine, Maltose, Sorbitol, Propylene
glycol
28. Contd...
• Urinary AG interpretation
• Positive UAG = Renal causes of NAGMA
• Normal or negative UAG = GI causes of NAGMA
29. High anion gap Normal anion gap
MUD PILES
•Methanol and other toxic alcohols
•Uremia
•Diabetic (or other) ketoacidosis
•Pyro glutamic acidosis
•Iron overdose
•Lactic acidosis
•Ethylene glycol
•Salicylates
PANDA RUSH
•Pancreatic secretion loss
•Acetazolamide
•Normal saline intoxication
•Diarrhea
•Aldosterone antagonists
•Renal tubular acidosis Type 1 (distal)
•Ureteric diversion
•Small bowel fistula
•Hyper alimentation (TPN)
30. Consequence of Metabolic Acidosis
Cardiovascular consequences:
• Decreased cardiac output
• Increased propensity to arrhythmias
• Decreased systemic vascular tone and arterial vasodilation
• Decreased responsiveness to catecholamines
• Pulmonary vasoconstricition
31. Consequence of Metabolic Acidosis
Respiratory consequences:
• Increased respiratory stimulus
• Increased work of breathing
• Right shift of the oxyhaemoglobin dissociation curve
(i.e. a decreased affinity of haemoglobin for oxygen)
32. Consequence of Metabolic Acidosis
Effects on renal function and fluid balance
• Increased renal ammonia production
• Increased renal tubular ammonia secretion
• Thus, increased renal oxygen demand
• Diuresis (eg. due to osmotic effect of "gap" anions)
33. Consequence of Metabolic Acidosis
Gastrointestinal consequences
• Decreased stomach emptying
• Nausea and vomiting
• Decreased splanchnic perfusion
34. Consequence of Metabolic Acidosis
Haematological consequences
• Coagulopathy (due to impaired clotting factor
function) -
• Impaired platelet aggregation (due to effects of
hyperchloraemia)
36. Metabolic Alkalosis
Initiating process Maintenance process
Gain of bicarbonate
•endogenous: metabolism of ketoacids
•exogenous: citrate, NaHCO3, lactate, antacid
Loss of acid
•Renal: diuretics
•GI: vomiting, nasogastric losses
•Hypochloraemia
•Hypokalaemia
•Hypomagnasaemia
•Volume contraction
•Corticosteroids (endogenous or exogenous)
37. Causes
Anions Cations
Chloride depletion
•Gastric losses by vomiting or drainage
•Diuretics: loop or thiazides
•Diarrhoea
•Posthypercapneic state
•Dietary chloride deprivation
•Gastrocystoplasty
•Cystic fibrosis (loss due to high sweat chloride content)
Bicarbonate excess (real or apparent)
•Iatrogenic alkalinisation
•Recovery from starvation
•Hypoalbuminemia
Potassium depletion
•Primary hyperaldosteronism
•Mineralocorticoid oversupplementation
•Licorice (glycyrrhizic acid)
•β-lactam antibiotics
•Liddle syndrome
•Severe hypertension
•Bartter and Gitelman syndromes
•Laxative abuse
•Clay ingestion
Calcium excess
•Hypercalcemia of malignancy
•Milk-alkali syndrome
38. Consequence of Metabolic Alkalosis
Respiratory consequences:
• Decreased respiratory drive stimulus
• Thus, pulmonary atelectasis
• Increased V/Q mismatch due to impared hypoxic
pulmonary vasoconstriction
• Left shift of the oxyhaemoglobin dissociation curve
39. Consequence of Metabolic Alkalosis
Cardiovascular consequences:
• Decreased cardiac output due to decreased
contractility
• Arrhythmias
40. Consequence of Metabolic Alkalosis
Neurological consequences
• Neuromuscular overexcitability
• Decreased cerebral blood flow due to cerebral
vasoconstriction
• Seizures
43. Causes of Respiratory Acidosis and
Alkalosis
Respiratory Acidosis Respiratory Alkalosis
•Increased inspired fraction of CO2
• Rebreathing of CO2-containing expired gas
• Addition of CO2 to inspired gas
• Insufflation of CO2 into body cavity (eg for laparoscopic surgery)
•Decreased alveolar ventilation
CO2 increases by 3mmg for every minute of apnoea
• central respiratory depression eg. by drugs or post-ictally
• neuromuscular disorders resulting in weakness
• lung or chest wall defects resulting in restriction
• airway obstruction, eg. after a seizure
• inadequate mechanical ventilation
•Increased metabolic CO2 production
• Malignant hyperthermia
• Thyrotoxicosis
• Phaeochromocytoma
• Sepsis
• Liver failure
• Extremes of physical exertion
• Convulsive epilepsy
•Respiratory control centre
• Head injury, stroke
• Anxiety, fear, stress, pain
• Salicylates
• Pregnancy
• Chronic liver disease
• Hypoxia
•Pulmonary receptors
• Pulmonary embolism
• Pneumonia
• Asthma
• Pulmonary oedema
44. Consequence of Respiratory
Acidosis
Respiratory consequences:
• Increased respiratory stimulus (maximum at 65mmHg)
• Increased work of breathing
• Alveolar hypoxia (on room air)
• Right shift of the oxyhaemoglobin dissociation curve
• With a chronically raised PaCO2, a decrease in 2,3-DPG
drives the curve back to the left
50. Step 9 Oxygenation
• Alveolar Gas Equation
• PAO2 = FiO2 x ( Atm. Pressure - Vapour pressure) -
(PaCO2 / RQ)
• a/A ratio should be more than 75%
• Normal P(A-a)O2 should be (Age in years / 4) + 4
51.
52. Step 10 Oxygen carrying capacity
• Calculate p50(st) - p50
• It reflects magnitude of bohr's effect and temperature
on ODC
• Normal p50(st) and abnormal p50 = shift in curve is
bcoz of pH PCO2 and Temp
• If both are abnormal and approximately equal = shift
is secondary to dyshemoglobins or 2,3-DPG levels
