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Learning Objectives Clinical Implications of Acid Base Balance.

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Presentation on theme: "Learning Objectives Clinical Implications of Acid Base Balance."— Presentation transcript:

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2 Learning Objectives Clinical Implications of Acid Base Balance

3 Terms Acid Any substance that can yield a hydrogen ion (H+) or hydronium ion when dissolved in water Release of proton or H+ Base Substance that can yield hydroxyl ions (OH-) Accept protons or H+ pH Negative log of the hydrogen ion concentration Represents the hydrogen concentration

4 Terms Normal pH is 7.35-7.45 Acidosis Alkalosis pH less than 7.35
pH greater than 7.45

5 For optimal functioning of cells…
Acids and bases in the body must be in balance

6 The Body and pH Homeostasis of pH is tightly controlled as pH has an effects on: Protein function Enzyme function Hormones Electrolyte Balance (Na+, K+, Cl-)

7 2 Important Questions Why does body pH change?
How does body resist change in pH?

8 Changes in pH We all consume every day food and drinks which contain acids, metabolism produces also acids...

9 PH IS CONSTANTLY ALTERED BY METABOLISM

10 You get acidotic every day !
While living, eating and drinking...there is.. Production of 1 mmol of fixed acid/kg body weight per day (60 kg=60 mmol/day)

11 Body pH Balance Maintained by chemical and physiologic buffer systems
Resist change in pH Buffer pairs – weak acid and a base Exchange a strong acid or base for a weak one Take up H+ or release H+ as conditions change

12 Buffer Systems

13 Organs involved in the regulation of Acid-Base Balance
CO2 production from complete oxidation of substrates 20% of the body’s daily production metabolism of organic acid anions such as lactate, ketones and amino acids metabolism of ammonium conversion of NH4+ to urea in the liver results in an equivalent production of H+ Production of plasma proteins esp. albumin contributing to the anion gap Bone inorganic matrix consists of hydroxyapatite crystals (Ca10(PO4)6(OH)2] bone can take up H+ in exchange for Ca2+, Na+ and K+ (ionic exchange) or release of HCO3-, CO3- or HPO42-

14 Organs involved in the regulation of Acid-Base Balance
Equilibrium with plasma High buffer capacity Haemoglobin – main buffer for CO2 Excretion of CO2 by alveolar ventilation: minimally 12,000 mmol/day Reabsorption of filtered bicarbonate: 4,000 to 5,000 mmol/day Excretion of the fixed acids (acid anion and associated H+): about 100 mmol/day

15 pH is determined by CO2 tension and HCO3
Kidney works by 2 mechanisms: Bicarbonate reabsorption Acid Secretion

16 Rates of correction Buffers function: almost instantaneously
Respiratory mechanisms: take several minutes to hours Renal mechanisms: may take several hours to days

17 Interpretation of ABGs

18 Interpretation of ABGs
Respiratory failure Type 1 Type 2 Acid base disorder Acidosis Alkalosis

19 NORMAL VALUES pH = 7.35 - 7.45 ( 7.4 ) pCO2 = 33 - 45 ( 40 ) mEq/L
HCO3 = ( 24 ) mEq/L pO2 = mmHg

20 Interpretation of ABGs
Respiratory failure Type 1; pO2 low Type 2; pO2 low, pCO2 high

21 Respiratory Alkalosis
Respiratory Acidosis Respiratory Alkalosis Metabolic Acidosis Metabolic Alkalosis Acid Base disorder

22 BASIC CONCEPTS pH~ CO2 ↔ H2CO3 ↔ H+ HCO3

23 Respiratory Acidosis pH~ PATHOGENESIS Retention of CO2

24 Respiratory Acidosis Causes Anatomical Site Disorder
CNS depression of resp.centre trauma, barbiturate Upper airway obstruction; Acute epiglotitis croup Resp. muscles paralysis ALS, phrenic nerve injury, GBS, poliomyelitis, hypokalemia, hypophsphatemia( ATP) Lungs obstructive diseases; chronic bronchitis, cystic fibrosis other; pulmonary edema, ARDS, RDS, severe bronchial asthma

25 Respiratory Acidosis COMPENSATION Metabolic alkalosis
HCO3 < 30 mEq/L in acute respiratory acidosis HCO3 > 30 mEq/L in chronic respiratory acidosis CALCULATION OF EXPECTED COMPENSATION Acute resp. acidosis ∆HCO3=0.1 X ∆pCO2 Chronic resp. acidosis ∆HCO3=0.4 X ∆pCO2

26 Respiratory Acidosis EXAMPLE pH= 7.2 pCO2= 74 HCO3= 27
∆HCO3=0.1 X ( 74-40) ∆HCO3=0.1 X 34 ∆HCO3=3.4 Expected HCO3=24+3.4=27.4

27 Respiratory Acidosis EXAMPLE pH= 7.34 pCO2= 60 HCO3= 32
∆HCO3=0.4 X ( 60-40) ∆HCO3=0.4 X 20 ∆HCO3=8 Expected HCO3=24+8=32

28 Case study 1 Arterial blood gas analysis reveals:
A 21-year-old woman is thrown from her horse at a local event. On the way to hospital she has become increasingly drowsy and the paramedics have inserted an oropharyngeal airway and given high flow oxygen via a face- mask. An arterial blood gas sample has been taken. Arterial blood gas analysis reveals: Inspired oxygen % (FiO2 0.4) PaO kPa >10 kPa (75 mmHg) on air pH – 7.45 PaCO kPa – 6.0 kPa Bicarbonate mmol/ l – 26 mmol l-1 Base excess mmol/l /- 2 mmol l-1

29 Case study A 65-year-old man with severe COPD has been found collapsed in the respiratory unit. On initial assessment by the ward nurse he is apnoeic but has an easily palpable carotid pulse. The nurse is attempting to ventilate his lungs with a bag-mask and supplemental oxygen (with reservoir) and has called the cardiac arrest team. On arrival: Oropharyngeal airway, ventilated with bag-mask, oxygen at 15 l min-1, Carotid pulse palpable, 90/ min, SpO2 99%,Comatosed (GCS 3) Arterial blood gas analysis reveals: Inspired oxygen % (FiO2 0.85) estimated PaO kPa (147 mmHg) >10 kPa (75 mmHg) on air pH – 7.45 PaCO kPa (135 mmHg) – 6.0 kPa (35 – 45 mmHg) HCO mmol/ l – 26 mmol/ l BE mmol/ l /- 2 mmol/ l

30 Respiratory Alkalosis
pH~ PATHOGENESIS Elimination of CO2

31 Respiratory Alkalosis
Causes Anatomical Site Disorder CNS over stimulation of resp.centre anxiety, high altitude, pregnancy, salicylate poisoning, endotoxic shock, cirrhosis Resp. muscles rib fracture; hyper ventilate from pain Lungs restrictive diseases; sarcoidosis, asbestosis, others; pulmonary embolus, mild bronchial asthma

32 Respiratory Alkalosis
COMPENSATION Metabolic acidosis HCO3 > 18 mEq/L in acute respiratory alkalosis HCO3 < 18 but >12 mEq/L in chronic respiratory alkalosis CALCULATION OF EXPECTED COMPENSATION Acute resp. alkalosis ∆HCO3=0.2 X ∆pCO2 Chronic resp. alkalosis ∆HCO3=0.5 X ∆pCO2

33 Respiratory Alkalosis
EXAMPLE pH= pCO2= 24 HCO3= 21 ∆HCO3=0.2 X ( 40-24) ∆HCO3=0.2 X 16 ∆HCO3=3.2 Expected HCO3=24-3.2=20.8

34 Respiratory Alkalosis
EXAMPLE pH= pCO2= 18 HCO3= 13 ∆HCO3=0.5X ( 40-18) ∆HCO3=0.5 X 22 ∆HCO3=11 Expected HCO3=24-11=13

35 Metabolic Acidosis pH~ PATHOGENESIS
Addition of an acid ( increased anion gap ) Loss of HCO3 or inability to synthesize HCO3( normal anion gap )

36 Metabolic Acidosis COMPENSATION Resp. alkalosis
CALCULATION OF EXPECTED COMPENSATION ∆pCO2 =1.2 X ∆HCO3 +/- 2

37 Metabolic Acidosis EXAMPLE pH= 7.27 pCO2= 27 HCO3= 12
∆pCO2 =1.2 X ∆ HCO3 +/- 2 ∆pCO2 =1.2 X ( 24-12) +/- 2 ∆pCO2 =1.2 X 12 +/- 2 ∆pCO2 = /- 2 Expected pCO2= 40 – 14.4= /- 2= 23.6 to 27.6

38 Metabolic Acidosis INCREASED ANION GAP TYPE Formula
AG= serum Na – (serum Cl + serum HCO3 )= 12 +/- 2 Example Na = 130 ( ) Cl = 88 ( 95 – 105 ) HCO3 = ( 22 – 28 ) AG= 130 – ( 88+10) = 130 – 98= 32

39 Metabolic Acidosis INCREASED ANION GAP TYPE Causes Lactic acidosis
Ketoacidosis Renal failure ( retention of organic acids) Salicylate poisoning Ethylene glycol poisoning Methyl alcohalpoisoning

40 Metabolic Acidosis NORMAL ANION GAP TYPE Formula
AG= serum Na – (serum Cl + serum HCO3 )= 12 +/- 2 Example Na = 136 ( ) Cl = ( 95 – 105 ) HCO3 = 14 ( 22 – 28 ) AG= 136 – ( ) = 136 –124= 12

41 Metabolic Acidosis NORMAL ANION GAP TYPE CAUSES Diarrhoea
Cholestyramine Drainage of bile or pancreatic secretions Type 1 distal renal tubular acidosis Type 11 proximal renal tubular acidosis Type IV renal tubular acidosis

42 Case study An 18-year-old insulin dependent diabetic is admitted to the emergency department. He has been vomiting for 48 h and because he was unable to eat, he has taken no insulin. On arrival: Breathing spontaneously, RR 35 min-1, oxygen 4 l min-1 via Hudson mask, SpO2 98% P 130 min-1, BP 90/65 mmHg GCS 12 (E3, M5, V4) Arterial blood gas analysis reveals: Inspired oxygen 30% (FiO2 0.3) estimated PaO kPa (129 mmHg) >10 kPa (75 mmHg) on air pH – 7.45 PaCO kPa (19 mmHg) 4.7 – 6.0 kPa (35 – 45 mmHg) HCO3 4.7 mmol/ l 22 – 26 mmol/ l BE mmol/ l +/- 2 mmol/ l The blood glucose is 30 mmol l-1 and there are ketones +++ in the urine.

43 Metabolic Alkalosis pH~ PATHOGENESIS Loss of hydrogen ion Gain of HCO3

44 Metabolic Alkalosis COMPENSATION Resp. acidosis
CALCULATION OF EXPECTED COMPENSATION ∆pCO2 =0.7 X ∆ HCO3 +/- 2

45 Metabolic Alkalosis EXAMPLE pH= 7.58 pCO2= 49 HCO3= 39
∆pCO2 =0.7 X ∆ HCO3 +/- 2 ∆pCO2 =0.7 X ( 39-24) +/- 2 ∆pCO2 =0.7 X 15 +/- 2 ∆pCO2 =10.5 +/- 2 Expected pCO2= = /- 2= 48.5 to 52.5

46 Metabolic Alkalosis CAUSES Vomiting Mineralocorticoid excess
Thiazide and loop diuretics

47 Calculate expected compensation
5 easy steps Look at pO2 Look at pH Look at pCO2 Look at HCO3 Calculate expected compensation

48 Type 1; pO2 low Type 2; pO2 low, pCO2 high Respiratory failure
5 easy steps Respiratory failure Type 1; pO2 low Type 2; pO2 low, pCO2 high Look for pO2

49 5 easy steps 2. Look for pH pH acidosis pH alkalosis

50 5 easy steps 3. Look for pCO2 pCO2 acidosis pCO2 alkalosis

51 5 easy steps 4. Look for HCO3 HCO3 acidosis HCO3 alkalosis

52 5 easy steps 5. Calculate for expected compensation
If compensation within expected range one primary disorder If compensation outside normal range more than one primary disorder

53 uncompensated disorder
5 easy steps 5. Compensation uncompensated disorder expected compensation in normal range partially compensated disorder Expected compensation moves outside the normal range, But does not bring pH in normal range full compensation and brings pH in normal range

54 Primary disorder pH pCO2 HCO3 Respiratory acidosis Respiratory alkalosis Metabolic acidosis Metabolic alkalosis

55 Example EXAMPLE pO2= 76 pH= 7.2 pCO2= 84 HCO3= 28.3

56 SOLUTION Type 2 respiratory failure
EXAMPLE Po2= 76 pH= 7.2 pCO2= 84 HCO3= 28.3 Type 2 resp. failure Acidosis Respiratory acidosis Metabolic compensation Calculation forexpected compensation ∆HCO3=0.1 X ( 84-40) ∆HCO3=0.1 X 44 ∆HCO3=4.4 Expected HCO3=24+4.4=28.4 Type 2 respiratory failure Partially compensated acute respiratory acidosis

57 p02 THANK YOU pH~


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