Acid and Base Balance

Dr Sanjay De Bakshi MS;FRCS USERNAME:- CMRI PASSWORD:- SDB123

INTERPRETATION OF BLOOD GASES

‘NORMAL’ BLOOD GASES pH PaO 2 PaCO 2 HCO 3 Base deficit or excess 7.35 – 7.45

13kPa 5.3kPa

22 – 25mmol/l -2 to +2 mmol/l

INTERPRETING BLOOD GASES

• Look at the PaO 2. Is the patient hypoxaemic? • What is the A-a gradient {Alveolar Arterial oxygen difference (A-a)DO 2 } • (A-a)DO 2 = FiO 2 x (atmospheric pressure – SVP of water) – PaCO 2 – PaO 2 . • (A-a)DO 2 =(FiO 2 x{101-6.2}-PaCO 2 -PaO 2 APACHE

SCORE RESULT

+4 >66.6

+3 46.7 66.5

+2 26.7 46.5

+1 0 <26.7

INTERPRETING BLOOD GASES • Look at the PaCO

2.

• Look at the pH. Alkalotic or Acidic?

INTERPRETING BLOOD GASES

DISTURBANCE OF ACID-BASE BALANCE cPaCO 2 = pH PaCO 2 DOES NOT CORRESPOND TO CHANGES cPaCO 2 = pH pH ‘NORMAL’ BLOOD GASES 7.35 – 7.45

PaO 2 PaCO 2 HCO 3 Base deficit or excess 13kPa 5.3kPa

22 – 25mmol/l -2 to +2 mmol/l HIGH IF ACIDOTIC LOW IF ALKALOTIC RESPIRATORY BASE DEFICIT ACIDOTIC = BASE DEFICIT CORRESPONDS TO CHANGES SBE = pH ALKALOTIC = BASE EXCESS SBE = pH METABOLIC DOES NOT CORRESPOND TO CHANGES MIXED

Respiratory acidosis

clinical disturbance that is due to alveolar dioxide occurs rapidly, and failure of ventilation promptly increases the partial (PaCO2). The reference range for PaCO2 is 36-44. Alveolar hypoventilation leads to an HCO3-/PaCO2 and decreases pH. What are the types of Respiratory Failure?

RESPIRATORY FAILURE

TYPE I FAILURE   HYPOXIC PaO2 < 8kPa   NORMAL OR LOW PaCO2

Impaired alveolar function; pneumonia,pulmonary oedema; ARDS

TYPE II FAILURE   HYPERCAPNIC PaO2 <8kPa   PaCO2 > 8kPa

Impaired alveolar ventilation; COPD, airway impairment,chest wall deformity, neuromuscular conditions

Compensation in Respiratory acidosis

• In acute respiratory acidosis, compensation occurs in 2 steps. • The initial response is in PaCO2. renal compensation cellular buffering that occurs over minutes to hours. Cellular buffering elevates plasma bicarbonate (HCO3-) only slightly, approximately 1 mEq/L for each 10-mm Hg increase • In chronic respiratory acidosis, the second step is 10 mm Hg in PaCO2. that occurs over 3-5 days. With renal compensation, renal excretion of carbonic acid is increased and bicarbonate reabsorption is increased. In renal compensation, plasma bicarbonate rises 3.5 mEq/L for each increase of

Respiratory acidosis

The expected change in serum bicarbonate concentration in respiratory acidosis can be estimated as follows: • Acute respiratory acidosis in PaCO PaCO 2 .

2 . : HCO • Chronic respiratory acidosis 3 : HCO increases 1 mEq/L for each 10-mm Hg rise 3 rises 3.5 mEq/L for each 10-mm Hg rise in

Respiratory alkalosis

• Respiratory alkalosis is a clinical disturbance due to alveolar hyperventilation. Alveolar hyperventilation leads to a decreased PaCO2 level (hypocapnia). In turn, the decrease in PaCO 2 level increases the ratio of bicarbonate concentration (HCO 3 ) to PaCO 2 and increases the pH level. Hypocapnia develops when the lungs remove more carbon dioxide than is produced in the tissues.

Respiratory alkalosis

Respiratory alkalosis can be acute or chronic. • In acute respiratory alkalosis the serum level is alkalemic. , the PaCO2 level is below the lower limit of normal and • In chronic respiratory alkalosis , the PaCO2 level is below the lower limit of normal, but the pH level is normal or near normal because of renal compensation.

Respiratory alkalosis

• Acute hyperventilation with hypocapnia causes a small early reduction in serum bicarbonate due to cellular uptake of bicarbonate. Acutely, plasma pH and bicarbonate concentration vary proportionately with the PaCO2 along a range of 15-40 mm Hg. • After a period of 2-6 hours, respiratory alkalosis is compensated by the kidneys by a decrease in bicarbonate reabsorption.

Respiratory alkalosis

• The expected change in serum bicarbonate concentration ([HCO 3 ]) can be estimated as follows: • Acute - [HCO 3 ] falls 2 mEq/L for each decrease of 10 mm Hg in the PaCO 2 (Limit of compensation: [HCO 3 ] = 12-20 mEq/L) • Chronic - [HCO 3 ] falls 5 mEq/L for each decrease of 10 mm Hg in the PaCO 2 (Limit of compensation: [HCO 3 ] = 12-20 mEq/L)

CONTROL OF VENTILATION

NEURAL CONTROL OF VENTILATION VOLUNTARY AUTOMATIC CEREBRAL CORTEX PONS & MEDULLA CORTICO-SPINAL TRACT

Regulation of Ventilation

• Chemical Control • Non chemical Control ?

REGULATION OF VENTILATION

CHEMICAL CONTROL 1. CO2 - via CSF H + CONCENTRATION 2. O2 - via CAROTID AND AORTIC BODIES 3. H+ - via CAROTID AND AORTIC BODIES NON CHEMICAL CONTROL 1. Afferents from Pons, Hypothalamus & Limbic System.

2. Afferent from Proprioceptors.

3. Afferents from pharynx, trachea & bronchi.

4. Vagal efferents from inflation/ deflation receptors in lung.

5. Afferents from baroreceptors: arterial, atrial, ventricular & pulmonary.

INTERPRETING BLOOD GASES

DISTURBANCE OF ACID-BASE BALANCE PaCO 2 cPaCO 2 = pH TO CHANGES DOES NOT CORRESPOND TO CHANGES cPaCO 2 = pH pH ‘NORMAL’ BLOOD GASES 7.35 – 7.45

PaO 2 PaCO 2 HCO 3 Base deficit or excess 13kPa 5.3kPa

22 – 25mmol/l -2 to +2 mmol/l HIGH IF ACIDOTIC LOW IF ALKALOTIC RESPIRATORY BASE DEFICIT ACIDOTIC = BASE DEFICIT CORRESPONDS TO CHANGES SBE = pH ALKALOTIC = BASE EXCESS SBE = pH METABOLIC DOES NOT CORRESPOND TO CHANGES MIXED

METABOLIC CHANGES ACIDOSIS

EFFFECTS OF METABOLIC ACIDOSIS o Increased respiratory drive (?){pH <7.1}.

o Decreased response to inotropes.

o H + ions into cells and K + out as buffering action.

o Hyperkalaemia.

ANION GAP

• The formula (Anion Gap = Na + - HCO metabolic acidosis.

3 - Cl ).

• Also important to define the TYPE of

METABOLIC CHANGES

Anion Gap = Na + (HCO3 + Cl ) CAUSES OF METABOLIC ACIDOSIS

Accumulation of H+ Anion gap > 8 mmols/l

Ketoacidosis

Loss of bicarbonate Anion gap < 8mmols/l

Vomiting /diarrhoea Lactic acidosis ARF Small bowel fistula Renal tubular acidosis Salicylate poisoning Calculating NaHCO 3 = ½ x base deficit(mmols/l x weight(kg) 3 Very rarely needed!!!!!

COMPENSATORY MECHANISMS

1. BLOOD - Buffers.

2. RESPIRATORY – increased ventilation – CO 2 blown off.

3. KIDNEYS – HCO 3 secreted all reabsorbed.

BUFFERS IN BLOOD

• Plasma proteins.

• Imidazole groups of the histidine residues of haemoglobin.

• Carbonic acid bicarbonate system.

• Phosphate system (intracellular) Therefore use of bicarbonate only for the pH < 7.2 in an inotrope resistant hypotensive patient

METABOLIC CHANGES ALKALOSIS

EFFFECTS OF METABOLIC ALKALOSIS o Reduced respiratory drive. o H+ ions out of cells and K+ in as buffering action.

o Hypokalaemia.

o Hypocalcaemia – tetany, paresthesia

COMPENSATORY MECHANISMS

1. RESPIRATORY – Reduced respiration = retention of CO 2 increased H + 2. RENAL – Increased HCO 3 = excretion

RELATION BETWEEN BASE EXCESS AND pCO2

• Whenever the pH is normal, i.e., pH = 7.4. then the PCO2 and the SBE are equal and opposite. In such circumstances, if the PCO2 is described as a marked acidosis then logically the SBE must be the exact opposite, a marked alkalosis. • Fortunately, the slope for BE/PCO2 when ph = 7.4 gives us this ratio: change in the PCO2.

• Thus, (change in) pCO 2 three units of change in the SBE is equivalent to a five mmHg : (change in) SBE = 5:3 • Therefore, chpCO 2 /chSBE=5/3

INTERPRETING BLOOD GASES

DISTURBANCE OF ACID-BASE BALANCE PaCO 2 cPaCO 2 = pH TO CHANGES DOES NOT CORRESPOND TO CHANGES cPaCO 2 = pH pH ‘NORMAL’ BLOOD GASES 7.35 – 7.45

PaO 2 PaCO 2 HCO 3 Base deficit or excess 13kPa 5.3kPa

22 – 25mmol/l -2 to +2 mmol/l HIGH IF ACIDOTIC LOW IF ALKALOTIC RESPIRATORY BASE DEFICIT ACIDOTIC = BASE DEFICIT CORRESPONDS TO CHANGES SBE = pH ALKALOTIC = BASE EXCESS SBE = pH METABOLIC DOES NOT CORRESPOND TO CHANGES MIXED

INTERPRETATION OF BLOOD GASES

‘NORMAL’ BLOOD GASES pH PaO 2 PaCO 2 HCO 3 Base deficit or excess 7.35 – 7.45

13kPa 5.3kPa

22 – 25mmol/l -2 to +2 mmol/l

EXAMPLES

Example A:

• pH = 7.2, • PCO2 = 60 mmHg, • SBE = 0 mEq/L ?

• • • • Overall change is acid. Respiratory change is also acid - therefore contributing to the acidosis. SBE is normal - no metabolic compensation. Therefore, pure Typical of acute respiratory acidosis

EXAMPLES

• •

Example B:

• pH = 7.35, • SBE = 7 mEq/L • • • PCO2 = 60 mmHg, ?

• • Overall change is slightly acid. Respiratory change is also acid therefore contributing to the acidosis. Metabolic change is alkaline therefore compensatory. The respiratory acidosis is 20 mmHg on the acid side of normal (40). To completely balance plus 20 would require 20 X 3 / 5 = 12 mEq/L SBE The actual SBE is 7 eEq/L, which is roughly half way between 0 and 12, i.e., a typical metabolic compensation. The range is about 6mEq/L wide - in this example between about 3 and 9 mEq/L. Magnitude: marked respiratory acidosis with moderate metabolic compensation

EXAMPLES

Example C:

• pH = 7.15, • SBE = -6 mEq/L

• •

• PCO2 = 60 mmHg,

• ?

• • Overall change is acid. Respiratory change is acid therefore contributing to the acidosis. Metabolic change is also acid therefore combined acidosis. The components are pulling in same direction - neither can be compensating for the other Magnitude: marked respiratory acidosis and mild metabolic acidosis

EXAMPLES

Example D:

• pH = 7.30, • PCO2 = 30

mmHg,

• SBE = -10

mEq/L

?

• • • • • • • Overall change is acid. Respiratory change is alkaline therefore NOT contributing to the acidosis. Metabolic change is acid - therefore responsible for the acidosis. The components are pulling in opposite directions. SBE is the acid component so it is primarily a metabolic problem with some respiratory compensation The metabolic acidosis is 10 mEq/L on the acid side of normal (0). To completely balance 10 would require 10 * 5 / 3 = 17 mmHg respiratory alkalosis (= 23 mmHg) The actual PCO2 is 30 eEq/L which is roughly half way between 23 and 40, i.e., a typical respiratory compensation. The range is about 10 mmHg wide - in this example between about 27 and 37 mmHg. Magnitude: marked metabolic acidosis with mild respiratory compensation.