ICU related topic

1. ARTERIAL BLOOD GAS
MODERATOR : DR KK Gupta
ASSO PROFF
PRESENTAR : DR SARAVANAKUMAR
PG Resident
Dept Of Anesthesia

2. ABG
• Arterial blood gas (ABG) sampling by direct vascular puncture is a
procedure often practiced in the hospital setting. The relatively low
incidence of major complications, its ability to be performed at the
patient’s bedside, and its rapid analysis make it an important tool
used by physicians to direct and redirect the treatment of their
patients, especially in patients who are critically ill at a specific point
in the course of a patient's illness.

3. Why is it Necessary to Order an ABG Analysis?
• Identification of respiratory, metabolic, and mixed acid-base
disorders.
• Therapeutic interventions such as mechanical ventilation in a patient
with respiratory failure, Head injury.
• Surgical evaluation (pulmonary resection).

4. Consideration
• An abnormal modified Allen test,
• Local infection or distorted anatomy
• The presence of arteriovenous fistulas or vascular grafts,
• Known or suspected severe peripheral vascular disease of the limb
involved.
• Coagulopathies or medium-to-high dose anticoagulation theraphy
(relative contraindication)

5. How would you time ABG sample?
• Must be done during steady state whenever there is initiation or
change in oxygen therapy or change in ventilatory parameters with
Pts on mech ventilation.
• In the patients without overt Pul disease a steady state is reached
between 3-10 minutes.
• In pts with chronic airway obstruction it takes about 20-30 minutes
after changes have been made.

6. • Antiseptic skin solution - Chlorhexidine and povidone-
iodine are solutions commonly used
• Syringe cap - Usually included in the ABG syringe kit
• Sterile gauze, 2 × 2 in.
• Adhesive bandage
• Bag with ice
• Sharp object container
• Lidocaine HCl 1% without epinephrine (optional)
• 25-gauge needle with syringe for local anesthetic
(optional)
Equipment

7. Procedure for arterial puncture
• Pt should be lying or sitting with arm well supported & clinician
seated if possible. Clean the skin around the site using institutional
protocol.
• A rolled towel positioned beneath the wrist helps hyperextended the
site while the pulse is carefully palpated. Sometimes palpating too
firmly can occlude the artery enough to prevent blood from flowing
into the syringe, even though the artery is punctured.

9. Do’s
• Communicate with the patient about the procedure.
• Always do Modified Allen test prior to drawing blood from a radial
artery.
• Apply pressure to the site for atleast 5 minutes or more if prolonged
CT.
• Keep ABG sample in an ice bag sample unless it is going to be
analysed within 10-15 minutes.

10. Don’ts
• Palpating too firmly
• Reposition a needle without first withdrawing the tip to subcutaneous
tissue.
• Leaving bubbles in an ABG syringes or draw air in before deairing.
• Fail to adequately heparinize a sample to prevent clotting (preferably
use preheparinized syringes for ABG collection. If available )

11. Precautions during ABG
•Delayed Analysis
Consumptiom of O2 & Production of CO2 continues after blood
drawn
Uniced sample quickly becomes invalid within 15-20
minutes
Iced Sample maintains values for 1-2 hour.
•PaCO2  3-10 mmHg/hour
•PaO2 
•pH  d/t lactic acidosis generated by glycolysis in R.B.C.

12. Air bubbles
PO2 150 mmHg & PCO2 0 mm Hg in air bubble(R.A.)
 Mixing with sample, lead to  PaO2 pH &  PaCO2
To avoid air bubble, sample drawn very slowly and preferabily in glass syringe.
Leucocytosis and Thrombocytosis
 pH and Po2 ; and  Pco2
0.1 ml of O2 consumed/dL of blood in 10 min in pts with N TLC
Marked increase in pts with very high TLC/plt counts – hence imm chilling/analysis
essential

13. Excessive heparin
Only .05-0.10 ml heparin(1000units/ml) required for 1 ml blood.
Use 2ml or less syringe with 25 gauge needle .
Dilutional effect on results  HCO3
- & PaCO2 .
Temperature
Patients Body Temperature affects the values of HCO3
- & PaCO2.
Any change in body temp at the time of sampling leads to alteration in
values detected by the electrodes.

14. Parameter 37 C (Change
every 10 min)
4 C (Change
every 10 min)
 pH 0.01 0.001
 PCO2 1 mm Hg 0.1 mm Hg
 PO2 0.1 vol % 0.01 vol %
Temp Effect On Change of ABG Values
Correcting patient temperature, once commonly applied to ABG sample,
especially in patients on CP bypass is no longer the standard as studies failed to show
Much clinical relevance of temperature –corrected PO2 values.

15. ABG Sample should always be sent with relevant information regarding FiO2 status
and Temp .

16. ABG provides us with rapid information on three physiological process.
1. Alveolar ventilation: is that portion of total ventilation that participates in gas
exchange with pul blood. The maintenance of CO2 level reflected by arterial CO2
tension (PaCO2) at any time depends on the quantity of CO2 produced in body
and its excretion through alveolar ventilation (VA).
Expressed by PaCO2 ˜ CO2 / VA.
On rearranging VA ˜ CO2 / PaCO2
Thus PaCO2 is the best index for assessment of alveolar ventilation.

17. 2. Oxygenation: This is a function of cardiopulmonary system and various factors
like arterial oxygen tension (PaO2), hemoglobin content and saturation with O2 and
CO. About 98% of O2is carried in blood in the combined state with Hb . Hypoxemia
is PaO2of less than 80mm Hg at sea level in an adult breathing room air. At cell
level it is called hypoxia.
Normal PaO2 : 95 – 100 mm Hg
Mild Hypoxemia : PaO2 60 – 80 mm Hg
Moderate Hypoxemia : PaO2 40 – 60 mm Hg
Severe Hypoxemia : PaO2 < 40 mm Hg
PaO2changes with age. PaO2= 104 – (0.27 * age) , roughly 1/3 of age subtracted
from 100.

18. PaO2 must always be interpreted in relation with Fio2 and age. PaO2 alone
doesn’t quantitate the physiological shunt, which helps in assessing the severity
of disease and guiding treatment.
PaO2at FiO2 .21% is 80 to 100 mm Hg.
Normal PaO2/FiO2 ratio are 400- 500 mm Hg.
Value < 200 most often indicates a shunt > 20%.

19. A-a gradient
It predicts the degree of shunt by comparing the partial pressure of O2 in the
alveoli(A) to that in the artery(a) i.e PAO2 -PaO2
PAO2 = FiO2(PATM- pH2O)- PaCO2/RQ
= 0.21(760- 47)- 40/0.8
= 100 mm Hg.
Normal A-a gradiant is 10-20 mmHg.
WHEN
• Patients with unexplained hypoxia.
• Patients with hypoxia exceeding the degree of their clinical illness.
WHY
The A-a Gradient can help determine the cause of hypoxia; it pinpoints the location
of the hypoxia as intra- or extra-pulmonary.

20. 3. Acid base disorder

21. Classification of Acid-Base Disorders
According to traditional concepts of acid-base physiology, the [H+] in
extracellular fluid is determined by the balance between the partial
pressure of carbon dioxide (PCO2) and the concentration of bicarbonate
(HCO3) in the fluid.
[H+] = 24* pCO2 / HCO3
The pCO2/HCO3 ratio identifies the primary acid-base disorders and
secondary responses,

22. Primary acid-base disorders
A change in either the PCO2 or the HCO3 will cause a change in the [H+]
of extracellular fluid.
respiratory acidosis
respiratory alkalosis
metabolic acidosis.
metabolic alkalosis.

23. Secondary Responses
• Secondary responses are designed to limit the change in [H+]
produced by the primary acid-base disorder, and this is accomplished
by changing the other component of the PaCO2/HCO3 ratio in the
same direction

24. STEPWISE APPROACH TO ACID-BASE ANALYSIS
• The reference ranges for arterial pH, PCO2, and HCO3 are shown
below.
pH = 7.36–7.44
PCO2 = 36–44 mm Hg
HCO3 = 22–26 mEq/L

25. Stage I: Identify the Primary Acid-Base
Disorder
• Rule 1
If the PaCO2 and/or the pH is outside the normal range, there is an acid-base
disorder.
• Rule 2
If abnormal, compare the directional change.
2A : If the PaCO2 and pH change in the same direction, there is a
primary metabolic acid-base disorder.
2B : If the PaCO2 and pH change in opposite directions, there is a
primary respiratory acid-base disorder.

26. Rule 2
What is the primary disorder?
What disorder is
present?
pH pCO2 HCO3
Respiratory Acidosis pH low high high
Metabolic Acidosis pH low low low
Respiratory Alkalosis pH high low low
Metabolic Alkalosis pH high high high

27. Stage I
Rule 1
• Look at the pH and pCO2: is outside the normal range?
EXAMPLE :
65yo M with CKD presenting with nausea, diarrhea and
acute respiratory distress
ABG : ABG 7.23/17/235 on 50% VM
BMP : Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.1
ACIDMEIA OR ALKALEMIA ????

28. ABG 7.23/17/235 on 50% VM
BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.1
Answer PH = 7.23 , HCO3 7
Acidemia

29. Rule 2
ABG 7.23/17/235 on 50% VM
BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.
• PH is low , CO2 is Low
• PH and PCO2 are going in same directions then its most
likely primary metabolic i.e metabolic acidosis.

30. • Rule 3
If only the pH or PaCO2 is abnormal, the condition is a mixed metabolic
and respiratory disorder (i.e., equal and opposite disorders).
3A : If the PaCO2 is abnormal, the directional change in PaCO2 identifies
the type of respiratory disorder (e.g., high PaCO2 indicates a
respiratory acidosis), and the opposing metabolic disorder.
3B : If the pH is abnormal, the directional change in pH identifies the
type of metabolic disorder (e.g., low pH indicates a metabolic
acidosis) and the opposing respiratory disorder.

31. Rule 3
The arterial pH = 7.38 and the PaCO2 = 55 mm Hg
only the PaCO2 is abnormal, so there is a mixed metabolic and
respiratory disorder. The PaCO2 is elevated, indicating a respiratory
acidosis, so the metabolic disorder must be a metabolic alkalosis.
Therefore, this condition is a mixed respiratory acidosis and metabolic
alkalosis. Both disorders are equivalent in severity because the pH is
normal.

32. Stage II: Evaluate the Secondary Responses
The goal in Stage II is to determine if there is an additional acid-base
disorder.
Secondary responses should not be called “compensatory responses”
because they do not completely correct the change in [H+] produced by
the primary acid-base disorder
Rule 4 : For a primary metabolic disorder, if the measured PaCO2 is
higher than expected, there is a secondary respiratory acidosis, and if
the measured PaCO2 is less than expected, there is a secondary
respiratory alkalosis

33. Is there appropriate secondary response ?
• Metabolic Acidosis
Δ PaCO2 = 1.2* Δ HCO3
Expected PaCO2 = 40-[1.2 *(24 - current HCO3)]
Winter’s formula: pCO2 = 1.5[HCO3] + 8 ± 2
• Metabolic Alkalosis
Δ PaCO2 = 0.7* Δ HCO3
Expected PaCO2 = 40+[0.7 *(current HCO3 -24)]

34. • Acute Respiratory Disorders
Acute respiratory acidosis:
Δ HCO3 = 0.1* Δ PaCO2
Expected HCO3 = 24+[0.1*(current PaCO2 – 40 )]
Acute respiratory alkalosis:
Δ HCO3 = 0.2* Δ PaCO2
Expected HCO3 = 24+[0.2*(40- current PaCO2 )]
• Chronic Respiratory Disorders
Chronic respiratory acidosis:
Δ HCO3 = 0.4* Δ PaCO2
Expected HCO3 = 24+[0.4*(current PaCO2 – 40 )]
chronic respiratory alkalosis:
HCO3 = 0.4* Δ PaCO2
Expected HCO3 = 24+[0.4*(40 – current PaCO2 )]

36. Rule 4
Consider a case
pH = 7.32,
PaCO2 = 23 mm Hg,
HCO3 = 16 mEq/L.
Here primary is METABOLIC ACIDOSIS the secondary response will be from
respiratory..so
Expected Δ PaCO2 = 1.2* Δ HCO3
PaCO2 = 40-[1.2 *(24 - current HCO3)]
Expected PaCO2 = 40 – [1.2×(24 – 16) ]= 30 mm Hg
Metabolic Acidosis with secondary Respiratory Alkalosis

37. Rule 5
For a primary respiratory disorder, a normal or near-normal HCO3
indicates that the disorder is acute
Rule 6
For a primary respiratory disorder where the HCO3 is abnormal,
indicates that the respiratory disorder is not acute.

38. RESPIRATORY
ACIDOSIS
ACUTE CHRONIC
For every ↑ 10 mm
Hg CO2
↑ 1 mmol/l HCO3
-
0.08 ↓ pH
↑ 4 mmol/l HCO3
-
0.03 ↓ pH
RESPIRATORY
ALKALOSIS
ACUTE CHRONIC
For every ↓ 10 mm
Hg CO2
↓ 2 mmol/l HCO3
-
0.08 ↑ pH
↓ 4 mmol/l HCO3
-
0.08 ↑ pH

39. ANION GAP
• The anion gap represents the "unmeasured" anions in the blood,
which are formed from organic acids that have dissociated in blood.
Unmeasured refers to the fact that these anions are not reported in a
standard metabolic panel or ABG but are contributing to the acidosis.

40. This electrochemical balance is expressed in the equation shown
below using electrolytes that are routinely measured, including sodium
(Na), chloride (CL), and bicarbonate (HCO3), as well as the
unmeasured cations (UC) and unmeasured anions (UA).
Total Serum Cations = Total Serum Anions
Na + (K + Ca + Mg) = HCO3 + Cl + (PO4 + SO4+ Protein +Organic Acids)
Na+ UC = (HCO3- + Cl) + UA
Anion Gap = Na - (HCO3- + Cl)
Normal Anion gap = 8-12

41. Influence of albumin
Albumin is the principal unmeasured anion, and the principal determinant
of the anion gap.
Albumin is a weak acid that contributes about 3 mEq/L to the AG for each
1 g/dL of albumin in plasma.
A low albumin level in plasma will lower the AG, and this could mask the
presence of an unmeasured anion (e.g., lactate) that is contributing to a
metabolic acidosis.
Since hypoalbuminemia is present in as many as 90% of ICU patients, the
following formula for the “corrected AG” (AGc) has been proposed to
include the contribution of albumin:
AGc = AG + 2.5*(4.5 - [albumin in g/dl])

42. An elevated AG occurs when there is an accumulation of fixed or non-volatile acids
(e.g., lactic acidosis), while a normal AG occurs when there is a primary loss of
bicarbonate
High AG Normal AG
Lactic acidosis Diarrhea
Ketoacidosis Isotonic saline infusion
End-stage renal failure Early renal insufficiency
Methanol ingestion Renal tubular acidosis
Ethylene glycol ingestion Acetazolamide
Salicylate toxicity ureteroenterostomy
The albumin-corrected AG (AGc) provides a more accurate assessment of metabolic acidosis than the AG

43. The Gap-Gap
In the presence of a high AG metabolic acidosis, it is possible to detect
another metabolic acid-base disorder
by comparing the AG excess to the HCO3 deficit
AG Excess/ HCO3 deficit = (AG - 12)/24 - HCO3
it is called Delta ratio

44. How is this useful?
• if one molecule of metabolic acid (HA) is added to the ECF and dissociates,
the one H+ released will react with one molecule of HCO3- to produce CO2
and H2O (buffering).
• the net effect will be an increase in unmeasured anions by the one acid
anion A- (ie anion gap increases by one) and a decrease in the bicarbonate
by one.
• if all the acid dissociated in the ECF and all the buffering was by
bicarbonate, then the increase in the AG should be equal to the decrease in
bicarbonate so the ratio between these two changes (which we call the
delta ratio) should be equal to one.
• the delta ratio quantifies the relationship between the changes in these
two quantities.

45. Example
• If the AG was say 26 mmols/l (an increase of 14 from the average
value of 12), it might be expected that the HCO3
-would fall by the
same amount from its usual value (ie 24 - 14 = 10mmols/l). If the
actual HCO3
- value was different from this it would be indirect
evidence of the presence of certain other acid-base disorders (see
Guidelines below)

46. ∆AG/ ∆HCO3 = 1 Pure High AG Met Acidosis
∆AG/ ∆HCO3 < 1 Assoc Normal AG Met Acidosis
∆AG/ ∆HCO3 > 1 Assoc Metabolic Alkalosis

47. Steps for ABG analysis
1. What is the pH? Acidemic or Alkalemic?
2. What is the primary disorder present?
3. Is there appropriate compensation?
4. Is the compensation acute or chronic?
5. Is there an anion gap?
6. If there is a AG, what is the delta gap?
7. What is the differential for the clinical processes?

48. Case 1
pH/pCO2/pO2 7.15/22/75 on room air, HCO3
- 9,
 anion gap = 10,
 albumin = 2.0
1: pH = Acidemia
2: pH and pCO2 in same direction
So Primary disturbance: Metabolic Acidosis
3 & 4: ∆ secondary response ?
Expected pCO2 = 1.5[HCO3] + 8 ± 2= 1.5(9)+8 21.5.
The expected pCO2is 21.5mmHg.
The actual pCO2 is 22, which is expected, so there is no concomitant disorder.

49. • 5: Anion Gap = 10
AGc = 10 + 2.5(4.5-2) = 16.5  Anion Gap Metabolic Acidosis
6: Delta Gap:
Delta gap = (AG - 12)/24 - HCO3
= (16.5-12) /24-9 = 0.3
which is < 0.4 so its a Non-AG Met Acidosis
ANION GAP METABOLIC ACIDOSIS with NON-ANION GAP METABOLIC
ACIDOSIS

50. Case 2
ABG 7.25/46/78 on 2L, HCO3
- 20, anion gap = 10, albumin = 4.5
1: pH = Acidemia
2. pH and pCO2 in opposite direction
So Primary disturbance: Acute Respiratory Acidosis
3 & 4. So ∆ secondary response ?
Expected HCO3 = 24+[0.1*(current PaCO2 – 40 )]
= 24+[0.1*(46-40)]= 24.6
The actual HCO3 is 20, which is lower than expected so, Metabolic acidosis is present
Anion Gap = 10 (alb normal so no correction necessary)
• Acute Respiratory Acidosis with Non Anion gap Metabolic acidosis

51. Case 3
• ABG 7.18/21/90 , HCO3
- = 7.8, anion gap = 10, albumin = 2.4,
Na+=140.6, cl- = 102
1. pH = Acidemia
2. pH and pCO2 in same direction
So Primary disturbance: Metabolic Acidosis
3 & 4. secondary response ?
Expected pCO2 = 1.5[HCO3] + 8 ± 2= 1.5(7.8)+8+2 21.7
The actual pCO2 is 21, which is expected, so there is no concomitant disorder.

52. 5. Anion Gap = 140.6 – (102+7.8) = 30.8
AGc = 30.8+ 2.5(4.5 – 2.4) =36.05
6. Delta gap = (36.05-12) /24-7.8 = 1.48
which is >1 so it is associated with Metabolic Alkalosis
ANION GAP METABOLIC ACIDOSIS with associated Metabolic alkalosis

53. Respiratory Alkalosis
Causes of Respiratory Alkalosis
Anxiety, pain, fever
Hypoxia, CHF
Lung disease with or without hypoxia – pulmonary embolus, reactive
airway, pneumonia
CNS diseases
Drug use – salicylates, catecholamines, progesterone
Pregnancy
Sepsis, hypotension
Hepatic encephalopathy, liver failure
Mechanical ventilation
Hypothyroidism
High altitude

54. Respiratory Acidosis
Causes of respiratory acidosis
CNS depression – sedatives, narcotics, CVA
Neuromuscular disorders – acute or chronic
Acute airway obstruction – foreign body, tumor, reactive airway
Severe pneumonia, pulmonary edema, pleural effusion
Chest cavity problems – hemothorax, pneumothorax, flail chest
Chronic lung disease – obstructive or restrictive
Central hypoventilation, OSA

55. Metobolic acidosis : Anion gap acidosis

56. Nongap metabolic acidosis
Causes of nongap metabolic acidosis - DURHAM
Diarrhea, ileostomy, colostomy, enteric fistulas
Ureteral diversions or pancreatic fistulas
RTA type I or IV, early renal failure
Hyperailmentation, hydrochloric acid administration
Acetazolamide, Addison’s
 For non-gap metabolic acidosis, calculate the urine anion gap
UAG = UNA + UK – UCL
 If UAG>0: renal problem
 If UAG<0: nonrenal problem (most commonly GI)

57. Metabolic alkalosis
Calculate the urinary chloride to differentiate saline responsive vs saline
resistant
Must be off diuretics in order to interpret urine chloride
Saline responsive UCL<10 Saline-resistant UCL >10
Vomiting If hypertensive: Cushings, Conn’s, RAS, renal failure
with alkali administartion
NG suction If not hypertensive: severe hypokalemia,
hypomagnesemia, Bartter’s, Gittelman’s, licorice
ingestion
Over-diuresis Exogenous corticosteroid administration
Post-hypercapnia

58. Thank you!