Abg

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ABG INTERPRETATION

STEPWISE APPROACH      



Obtain clues from the clinical setting Determine primary disorder Check the compensatory response Calculate the anion gap Calculate the delta/deltas Identify specific etiologies for the acidbase disorder Prescribe treatment

DETERMINE CLUES FROM THE CLINICAL SETTING

CLUES FROM CLINICAL SETTING HIGH ANION GAP METABOLIC ACIDOSIS Ketoacidosis – dm, alcohol, starvation INH, methanol, lactic acid Renal failure Hypotension

CLUES FROM CLINICAL SETTING NORMAL ANION GAP METABOLIC ACIDOSIS Diarrhea RTA Interstitial nephritis Early renal failure Urinary tract obstruction

CLUES FROM CLINICAL SETTING METABOLIC ALKALOSIS (urine Cl < 10 mEq/d) Vomiting Remote diuretic use Post hypercapnea Chronic diarrhea Cystic fibrosis

CLUES FROM CLINICAL SETTING METABOLIC ALKALOSIS (urine Cl > 10 mEq/d) Bartter’s syndrome Severe potassium depletion Current diuretic use Hypercalcemia Hyperaldosteronism Cushing’s syndrome

CLUES FROM CLINICAL SETTING RESPIRATORY ACIDOSIS CHRONIC: ACUTE:

COPD pneumonia

RESPIRATORY ALKALOSIS Hyperventilation

DETERMINE THE PRIMARY DISORDER

DETERMINE PRIMARY DISORDER 

Check the trend of the pH, HCO3, pCO2



The change that produces the pH is the primary disorder pH = 7.25

ACIDOSIS

HCO3 = 12 ACIDOSIS

METABOLIC ACIDOSIS

pCO2 = 30 ALKALOSIS

DETERMINE PRIMARY DISORDER 

Check the trend of the pH, HCO3, pCO2



The change that produces the pH is the primary disorder pH = 7.25

ACIDOSIS

HCO3 = 28 ALKALOSIS

pCO2 = 60 ACIDOSIS

RESPIRATORY ACIDOSIS

DETERMINE PRIMARY DISORDER 

Check the trend of the pH, HCO3, pCO2



The change that produces the pH is the primary disorder pH = 7.55

ALKALOSIS

HCO3 = 19 ACIDOSIS

pCO2 = 20 ALKALOSIS

RESPIRATORY ALKALOSIS

DETERMINE PRIMARY DISORDER 



If the trend is the same, check the percent difference The bigger %difference is the 10 disorder (16-24)/24 = 0.33 (60-40)/40 = 0.5 pH = 7.25

ACIDOSIS

HCO3 = 16 ACIDOSIS

pCO2 = 60 ACIDOSIS

RESPIRATORY ACIDOSIS

DETERMINE PRIMARY DISORDER 



If the trend is the same, check the percent difference The bigger %difference is the 10 disorder (38-24)/24 = 0.58 (30-40)/40 = 0.25 pH = 7.55

ALKALOSIS

HCO3 = 38 ALKALOSIS

pCO2 = 30 ALKALOSIS

METABOLIC ALKALOSIS

CHECK THE COMPENSATORY RESPONSE

COMPENSATORY RESPONSE HENDERSEN-HASSELBACH EQUATION 24 x pCO2 H = ---------------HCO3 Metabolic or Respiratory Acidosis

COMPENSATORY RESPONSE HENDERSEN-HASSELBACH EQUATION 24 x pCO2 H = ---------------HCO3 Metabolic or Respiratory Alkalosis

COMPENSATORY RESPONSE METABOLIC ACIDOSIS  pCO2 = HCO3 x 1.2 + 2 HCO3 =12

pCO2 =14.4 – 40 = 25.6

HCO3 =7

pCO2 =20.4 – 40 = 19.6

COMPENSATORY RESPONSE METABOLIC ALKALOSIS  pCO2 =  HCO3 x 0.7 + 2

HCO3 =35

pCO2 =7.7 + 40 = 47.7

HCO3 =40

pCO2 =11.2 + 40 = 51.2

COMPENSATORY RESPONSE ACUTE RESPIRATORY ACIDOSIS  HCO3 = pCO2 x 0.1

pCO3 =55

HCO3 =1.5 + 24 = 25.5

pCO3 =80

HCO3 =4 + 24 = 28

COMPENSATORY RESPONSE CHRONIC RESPIRATORY ACIDOSIS  HCO3 = pCO2 x 0.35

pCO3 =55 pCO3 =80

HCO3 =5.25 + 24 = 29.25 HCO3 =14 + 24 = 38

COMPENSATORY RESPONSE RESPIRATORY ALKALOSIS  HCO3 = pCO2 x 0.2

pCO3 =25

HCO3 =3 - 24 = 21

pCO3 =32

HCO3 =1.6 - 24 = 22.4

CALCULATE THE ANION GAP

ANION GAP Na – (HCO3 + Cl) = 12 + 4 Na = 135 Cl = 97

HCO3 = 15 RBS = 100 mg%

AG = 135 – 112 = 23

ANION GAP Na – (HCO3 + Cl) = 12 + 4 Na = 135 Cl = 97

HCO3 = 15 RBS = 500 mg%

Corrected Na = Na + RBS mg% -100 x 1.6 100 AG = 135 + 6.4 – 112 = 29.4

CHECK THE DELTA / DELTA

DELTA - DELTA 

If with high AG metabolic acidosis AG

 HCO3 

If with normal AG metabolic acidosis Cl HCO3

A high AG always indicates the presence of a HAG metabolic acidosis

DELTA - DELTA / = 1

Simple NAG metabolic acidosis

/ > 1

HAGMA/NAGMA + meta alk

/ < 1

HAGMA+NAGMA

CASE 1 56F with vomiting and diarrhea 3 days ago despite intake of loperamide. Her last urine output was 12 hours ago. PE showed BP = 80/60, HR = 110, RR = 28. There is poor skin turgor.

CASE 1 serum Na = 130 K = 2.5

pH = 7.30 pCO2 = 30

Cl = 105

HCO3 = 15

BUN = 15

pO2 = 90

crea = 177 RBS = 100 BCR = BUN / crea x 247.6 = 21

PRE-RENAL

CASE 1 serum Na = 130 K = 2.5

pH = 7.30 pCO2 = 30

Cl = 105

HCO3 = 15

BUN = 15

pO2 = 90

crea = 177 RBS = 100 pH = acidosis, pCO2 =alk, HCO3 = acidosis

Metabolic Acidosis

CASE 1 serum Na = 130 K = 2.5

pH = 7.30 pCO2 = 30

Cl = 105

HCO3 = 15

BUN = 15

pO2 = 90

crea = 177 RBS = 100 pCO2 = 9 x 1.2 = 10.8

Compensated Metabolic Acidosis

CASE 1 serum Na = 130 K = 2.5

pH = 7.30 pCO2 = 30

Cl = 105

HCO3 = 15

BUN = 15

pO2 = 90

crea = 177 RBS = 100 AG= 130 – (105+15) = 10

NAGMA

CASE 1 serum Na = 130 K = 2.5

pH = 7.30 pCO2 = 30

Cl = 105

HCO3 = 15

BUN = 15

pO2 = 90

crea = 177 RBS = 100 /= (105-100)/(24-15) = 0.56

NAGMA + HAGMA

CASE 1 56F with vomiting and diarrhea 3 days ago despite intake of loperamide. Her last urine output was 12 hours ago. PE showed BP = 80/60, HR = 110, RR = 28. There is poor skin turgor. pH 7.30, HCO3=15, pCO2=30, Na=130 K=2.5 How will you correct the acid base disorder?

CASE 1 1) Hydrate 2) Hydrate + IV NaHCO3 3) Hydrate + oral NaHCO3 4) Hydrate + correct hypokalemia

How will you correct the acid base disorder?

INDICATIONS FOR HCO3 THERAPY 

pH < 7.2 and HCO3 < 5 – 10 mmHg



When there is inadequate ventilatory compensation Elderly on beta blockers in severe acidosis with compromised cardiac function Concurrent severe AG and NAGMA Severe acidosis with renal failure or intoxication



 

COMPLICATIONS OF HCO3 THERAPY        

Volume overload Hypernatremia NaHCO3 50 ml = 45 mEq Na Hyperosmolarity NaHCO3 gr X tab = 7 mEq Na Hypokalemia Intracellular acidosis Causes overshoot alkalosis Stimulates organic acid production  tissue O2 delivery

POTASSIUM CORRECTION  

K deficit = (3.5 – K)/0.27 x 100 Give ½ of the deficit in 24 hours

K deficit = (3.5 – 2.5)/0.27 x 100 = 370 1 cc oral KCL = 1.33 mEq K 1 potassium durule = 10 mEq K

CASE 2 30M with epilepsy has a grand mal seizure. Labs showed: pH = 7.14 Na = 140 pCO2= 45 K=4 HCO3 = 17 %pCO2 =13, %HCO3 = 29

Cl = 98 Metabolic Acidosis

CASE 2 30M with epilepsy has a grand mal seizure. Labs showed: pH = 7.14 Na = 140 pCO2= 45 K=4 HCO3 = 17 pCO2 =7 x 1.2 = 8.4

Cl = 98 Metabolic & Respiratory Acidosis

CASE 2 30M with epilepsy has a grand mal seizure. Labs showed: pH = 7.14 Na = 140 pCO2= 45 K=4 HCO3 = 17 AG = 140 – (98+17) = 25

Cl = 98

HAGMA + RAc

CASE 2 30M with epilepsy has a grand mal seizure. Labs showed: pH = 7.14 Na = 140 pCO2= 45 K=4 HCO3 = 17 /= (25-12)/(24-17) = 1.9

Cl = 98

HAGMA + MAlk + RAc

CASE 2 30M with epilepsy has a grand mal seizure. Labs showed: pH = 7.14 Na = 140 pCO2= 45 K=4 HCO3 = 17

Cl = 98

How will you correct the acid base disorder?

CASE 2 1) IV NaHCO3 using HCO3 deficit 2) oral NaHCO3 at 1 mEq/kg/day 3) intubate 4) no treatment

How will you correct the acid base disorder?

CASE 2 HCO3 DEFICIT = (D –A) x 0.5 x kg BW HCO3 deficit = (18 – 17) x 0.5 x 60 = 30 As HCO3  < 5-10, the Vd increases; hence use 0.7 to 0.1

dHCO3 = 15 - 18 Maintenance 1 mEq/day

How you correct acid½base disorder? Give ½ will as bolus and thethe other as drip in 24 hrs

PRINCIPLES OF HCO3 THERAPY LACTIC ACIDOSIS    

Primary effort should be improving O2 delivery Use NaCO3 only when HCO3 < 5 mmol/L In states of  CO, raising the CO will have more impact on the pH In cases of low alveolar ventilation,  ventilation to lower the tissue pCO2

PRINCIPLES OF HCO3 THERAPY KETOACIDOSIS 



Rate of H+ production is slow; NaHCO3 tx may just provoke severe hypokalemia Should be given if… 1) severe hyperkalemia despite insulin 2) HCO3 < 5 mmol/L 3) worsening acidemia inspite of insulin

CASE 3 19F, fashion model, is surprised to find her K=2.7 mmol/L because she was normokalemic 6 months ago. She admits to being on a diet of fruit and vegetables but denies vomiting and the use of diuretics or laxatives. She is asymptomatic. BP = 90/55 with subtle signs of volume contraction.

CASE 3 serum Na K Cl HCO3 30 pH pCO2

Plasma 138 2.7 96

Urine 63 34 0 0

7.45 45

pH = alk, pCO2 =acidosis HCO3 = alkalosis

5.6

Metabolic Alkalosis

CASE 3 serum Na K Cl HCO3 30 pH pCO2

Plasma 138 2.7 96

Urine 63 34 0 0

7.45 45

pCO2 = 6 x 0.7 = 4.2

5.6 Compensated Metabolic Alkalosis

CASE 3 serum Na K Cl HCO3 30 pH pCO2

Plasma 138 2.7 96

Urine 63 34 0 0

7.45 45

AG= 138 – (96+30) = 12

5.6

NAG

CASE 3 serum Na K Cl HCO3 30 pH pCO2

Plasma 138 2.7 96

Urine 63 34 0 0

7.45 45

5.6

What is the cause of the acid base disorder?

CASE 3 1) diuretic intake 2) surreptitious vomiting 3) diuretic intake 4) Bartter’s syndrome 5) Adrenal tumor 6) nonreabsorbable anion How What should is the her cause acid-base of the disorder acid base bedisorder? managed?

CASE 3 1) correct hypokalemia 2) hydrate with NSS 3) administer acidyfing agent 4) give carbonic anhydrase inhibitor

How should her acid-base disorder be managed?

MANAGEMENT OF METABOLIC ALKALOSIS      

Chloride repletion Potassium repletion Tx hypermineralocorticoidism Dialysis Carbonic anhydrase inhibitors Acidyfing agents  HCl, NH4Cl

INDICATIONS OF HCl 





pH > 7.55 and HCO3 > 35 with contraindications for NaCl or KCl use Immediate correction of metabolic alkalosis in the presence of hepatic encephalopathy, cardiac arrhythmias, digitalis intoxication When initial response to NaCl, KCl, or acetalozamide is too slow or too little

USE OF HCl   

HCL requirement = (A – D) x 0.5 x kg BW 0.1 – 0.2 N HCl solution = 100 – 200 mEq Do not exceed 0.2 mEq/kg/hour of HCl

HCO3 = 70 wt = 60 kg

HCl = 1,380 mEq

CASE 4 73M with long standing COPD (pCO2 stable at 52-58 mmHg), cor pulmonale, and peripheral edema had been taking furosemide for 6 months. Five days ago, he had anorexia, malaise, and productive cough. He continued his medications until he developed nausea. Later he was found disoriented and somnolent

CASE 4 PE:

BP 110/70, HR 110, RR 24, T=40 respiratory distress prolonged expiratory phase postural drop in BP drowsy, disoriented scattered rhonchi and rales BLFs distant heart sounds trace pitting edema

CASE 4

admission serum Na hrs 136 K 3.2 Cl 78 HCO3 40 pH pCO2

7.33 78

pO2 43 pH = acidosis  pCO2 =acidosis, HCO3 = alk

after 48 139 3.9 86 38 7.42 61 56 Respiratory Acidosis

Respiratory Acidosis & M. Alkalosis

CASE 4

admission serum Na hrs 136 K 3.2 Cl 78 HCO3 40 pH pCO2

7.33 78

pO2

43

HCO3 = (55-40) x 0.35 = 5.25 HCO3 = (78-55) x 0.1 = 2.3

after 48 139 3.9 86 38 7.42 61 56 HCO3 = 24 + 5.25 + 2.3 = 31.55

CASE 4

admission serum Na hrs 136 K 3.2 Cl 78 HCO3 40

after 48 139 3.9 86 38

pH pCO2

7.33 78

7.42 61

pO2

43

56

How should this patient be managed?

CASE 4 1) intubation and mechanical ventilation 2) low flow oxygenation by nasal prong 3) oxygen by face mask 4) sodium bicarbonate infusion with KCl

How should this patient be managed?

MANAGEMENT OF RESPIRATORY ACIDOSIS 



  

Correct underlying cause for hypoventilation  effective alveolar ventilation  intubate, mechanically ventilate Antagonize sedative drugs Stimulate respiration (e.g. progesterone) Correct metabolic alkalosis

CASE 5 42M, alcoholic, brought to the ER intoxicated. He was found at Rizal park in a pool of vomitus. PE showed unkempt and incoherent patient with a markedly contracted ECF volume. T=390 C with crackles on the RULF.

CASE 5 serum Na = 130 K = 2.9 Cl = 80 BUN = 12 crea = 120 RBS = 15 mmol/L

pH = 7.53 pCO2 = 25 HCO3 = 20 pO2 = 60 alb = 38

BCR = (12/120) x 247.6 = 24.76

PRE-RENAL

CASE 5 serum Na = 130 K = 2.9 Cl = 80 BUN = 12 crea = 120 RBS = 15 mmol/L

pH = 7.53 pCO2 = 25 HCO3 = 20 pO2 = 60 alb = 38

%pCO2 =38, %HCO3 = 18

Respiratory Alkalosis

CASE 5 serum Na = 130 K = 2.9 Cl = 80 BUN = 12 crea = 120 RBS = 15 mmol/L HCO3 = (40-25) x 0.2 = 3

pH = 7.53 pCO2 = 25 HCO3 = 20 pO2 = 60 alb = 38 Compensated Respiratory Alkalosis

CASE 5 serum Na = 130 K = 2.9 Cl = 80 BUN = 12 crea = 120 RBS = 15 mmol/L AG = 130 – (80 + 20) = 30

pH = 7.53 pCO2 = 25 HCO3 = 20 pO2 = 60 alb = 38 HAGMA + RAlk

CASE 5 serum Na = 130 K = 2.9 Cl = 80 BUN = 12 crea = 120 RBS = 15 mmol/L

pH = 7.53 pCO2 = 25 HCO3 = 20 pO2 = 60 alb = 38

What are the causes of his acid base disturbance?

CASE 5 1) aspiration pneumonia 2) alcohol ketoacidosis 3) vomiting

What are the causes of his acid base disturbance?

MANAGEMENT OF RESPIRATORY ALKALOSIS 

 

Correct underlying cause of hyperventilation Rebreathe carbon dioxide Mechanical control of ventilation  increase dead space  decrease back up rate  decrease tidal volume  paralyze respiratory muscles

QUESTIONS?

Thank You

ACID BASE PHYSIOLOGY by: ROMMEL S. GAMBOA, M.D.

ACID BASE PHYSIOLOGY    

maintenance of constant blood pH physiologic buffers renal system respiratory system

BUFFERS 1. Extracellular buffers a. HCO3major extracellular buffer b. PO4minor extracellular buffer 2. Intracellular buffers a. Organic phosphates (AMP. ADP, ATP, 2,3DPG) b. Proteins (hemoglobin [major intracellular], DeoxyHgb, oxyHgb, imidazole and α-amino groups.

HENDERSON-HASSELBALCH EQUATION  

is used to calculate pH pH = pK + log [A-]/[HA-] pH = log of 10 [H] pK = log 10 equilibrium constant [A-] = base form of the buffer [HA] = acid form of the buffer

Techniques of obtaining a sample   

 



Materials The patient is seated or lying down The wrist should be extended approximately30 degrees A definite pulse should be palpated The site should be cleansed with 70% isopropyl alcohol The radial artery should again be palpated while holding the heparinized syringe much like a pencil or dart with the opposite hand.

Techniques of obtaining a sample 





The needle is then inserted opposite the blood flow at 45-degree angle or less with the bevel turned upward. After a 3-4 ml of sample is withdrawn, a sterile cotton is applied over the puncture site. Digital pressure should be applied for at least 5 minutes. The specimen must be placed on ice and transported within 15 minutes at 4ºC and tested immediately

NORMAL BLOOD GAS VALUES pH

pCO2 pO2

HCO3 BE

Hgb

O2Sat

Hi

7.45

45

100

26

+2

18

100

Lo

7.35

35

80

22

-2

12

90

TWO ORGAN SYSTEM INVOLED IN ACID-BASE PHYSIOLOGY  

Respiratory System Renal System

BLOOD GAS ANALYZERS 



determine acid-base balance through the measurement of partial pressure of oxygen, carbon dioxide and pH. Bicarbonate and other parameters are calculated from previously mentioned measurements

METABOLIC ACIDOSIS   



increase in arterial [H+] decrease in arterial [HCO3] respiratory compensation – hyperventilation (Kussmaul breathing) renal compensation - ↑ excretion of H+ as titratable acid and NH4; ↑ reabsorption of HCO3

METABOLIC ALKALOSIS  

 

decrease in arterial H+ ↑ HCO3 because of loss of H+ e.g. vomiting when H+ is lost from the stomach respiratory compensation: hypoventilation renal compensation: ↑ excretion of HCO3

RESPIRATORY ACIDOSIS 

  



caused by primary decrease in respiratory rate and retention of CO2 ↑ in H+ and HCO3 by mass action no respiratory compensation renal compensation: ↑ excretion of H+ and NH4 ↑ reabsorption of HCO3

RESPIRATORY ALKALOSIS 

  



caused by primary increase in respiratory rate and loss of CO2 ↓ H+ and HCO3 by mass action no respiratory compensation renal compensation: ↓ excretion of H+ and NH4 ↓ reabsorption of HCO3

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