The document discusses the importance of ABG (arterial blood gas) interpretation and physiotherapy recommendations for critically ill patients, particularly in the ICU. It emphasizes the necessity of careful monitoring and intervention strategies to enhance respiratory function, decrease length of stay, and improve patient outcomes. Key considerations include assessing hemodynamic status, the impact of positioning, and understanding metabolic and respiratory acid-base disorders.

1. ABG
INTERPRETATION
Reza Nejat, M.D.,
Anesthesiologist, FCCM,
Former Assistant Professor, SBMU
Bazarganan Hospital

2. ABG INTERPRETATION
 Recommendations for
Physiotherapy in the ICU
 Acute lobar atelectasis ♣♣
 Positioning in severe ARDS
 Side lying improves 0xygenation
 Continuous rotational therapy
 Facilitating weaning
 Decreasing length of stay in the ICU or
hospital,
 Reducing mortality or morbidity ♣♣
 Preventing loss of joint range or soft-
tissue length**

3. ABG INTERPRETATION
 Physiotherapy at ICU
 Positioning
 Mobilisation
 Manual hyperinflation (MHI)
 Percussion, manual or
mechanical vibration
 Airway suctioning
 Coughing
 Breathing exercise

4. ABG INTERPRETATION
 The physiotherapy treatment
prevents and reduces potential
pulmonary complications:
 Hypoventilation,
 Hypoxemia,
 Infection in order to restore
muscular and pulmonary function as
fast as possible.

5. ABG INTERPRETATION
 The side effects of
physiotherapy:
 Metabolic
 Hemodynamic
 ICP↑

6. ABG INTERPRETATION
𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑 = ↑ 𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎 𝒅𝒅𝒅𝒅𝒅𝒅𝒅𝒅𝒅𝒅𝒅𝒅
physiotherapist should have knowledge about:
𝒐𝒐𝒐𝒐𝒐𝒐𝒐𝒐𝒐𝒐𝒐𝒐 𝒅𝒅𝒅𝒅𝒅𝒅𝒅𝒅𝒅𝒅𝒅𝒅𝒅𝒅𝒅𝒅 𝒕𝒕𝒕𝒕 𝒕𝒕𝒕𝒕𝒕𝒕 𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄
𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄 𝒐𝒐𝒐𝒐𝒐𝒐𝒐𝒐𝒐𝒐𝒐𝒐 𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄

7. ABG INTERPRETATION
During invasive ventilation
 Physiotherapy might be associated with:
𝑽𝑽𝑽𝑽𝑽𝑽 ↑↑
𝑺𝑺𝑺𝑺𝑺𝑺𝑺𝑺𝑺𝑺𝑺𝑺𝑺𝑺𝑺𝑺𝑺𝑺𝑺𝑺𝑺𝑺 𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔 ↑
𝑾𝑾𝑾𝑾𝑾𝑾 ↑

8. ABG INTERPRETATION
 The metabolic and cardiovascular effects of
turning a patient into a side lying position are
greater than the physiological stress incurred
by the addition of physiotherapy treatment.
 Berney S and Denehy L (2003): Australian Journal of Physiotherapy 49: 99-105

9. ABG INTERPRETATION
 What should be done during
physiotherapy:
 Monitor hemodynamic status
 Sedation before physiotherapy
 Preoxygenation, sedation, and
reassurance before suction
 Monitor ICP and CPP

10. ABG INTERPRETATION
 Physiotherapy
ABG interpretation
???? Their relationship

11. ABG INTERPRETATION
∆Critically ill patients are in hyper-metabolic state∆
 The ABG allows to assess patients’:
 metabolic status
 respiratory status
 ability to cope with their illness.

12. ABG INTERPRETATION
 ABG is requested to determine:
 pH
 PaCO2
 PaO2
 ABG is used to assess:
 the effectiveness of:
 Gaseous Exchange
 Ventilation
 pH derangement=Abnormal cell metabolism

13. ABG INTERPRETATION
 when mobilization should be done:
 Physiotherapist should review medical
background
 Hemodynamic indices should be stable:
𝐻𝐻𝐻𝐻𝑟𝑟𝑟𝑟𝑟𝑟𝑟𝑟 < 𝐻𝐻𝐻𝐻𝑚𝑚𝑚𝑚𝑚𝑚50%
𝑆𝑆𝑆𝑆𝑆𝑆 100 – 140 𝑚𝑚𝑚𝑚𝑚𝑚𝑚𝑚
𝐷𝐷𝐷𝐷𝐷𝐷 80 − 105 𝑚𝑚𝑚𝑚𝑚𝑚𝑚𝑚
𝑣𝑣𝑣𝑣𝑣𝑣𝑣𝑣𝑣𝑣𝑣𝑣𝑣𝑣𝑣𝑣𝑣𝑣𝑣𝑣𝑣𝑣 𝑟𝑟𝑟𝑟𝑟𝑟𝑟𝑟𝑟𝑟𝑟𝑟𝑟𝑟𝑟𝑟 < 20%
𝑁𝑁𝑁𝑁𝑁𝑁𝑁𝑁𝑁𝑁𝑁𝑁 𝐸𝐸𝐸𝐸𝐸𝐸
 Respiratory stability:
𝑃𝑃𝑃𝑃𝑃𝑃2/𝐹𝐹𝐹𝐹𝐹𝐹2 > 150 – 𝑠𝑠𝑠𝑠𝑠𝑠𝑠𝑠𝑠𝑠𝑠𝑠𝑠𝑠 𝑖𝑖𝑖𝑖 𝑐𝑐ℎ𝑎𝑎𝑎𝑎𝑎𝑎
𝑃𝑃𝑃𝑃𝑃𝑃2/𝐹𝐹𝐹𝐹𝐹𝐹2 > 300 (30𝑚𝑚 𝑤𝑤𝑤𝑤𝑤𝑤𝑤𝑤𝑤𝑤𝑤𝑤𝑤𝑤)
𝑆𝑆𝑆𝑆𝑆𝑆2 > 90 𝑎𝑎𝑎𝑎𝑎𝑎 𝑟𝑟𝑟𝑟𝑟𝑟𝑟𝑟𝑟𝑟𝑟𝑟 𝑑𝑑𝑑𝑑𝑑𝑑𝑑𝑑𝑑𝑑𝑑𝑑𝑑𝑑𝑒𝑒 𝑖𝑖𝑖𝑖 𝑆𝑆𝑆𝑆𝑆𝑆2 < 4%

14. ABG INTERPRETATION
 Accurate and timely
interpretation of ABG and an
acid–base disorder can be
lifesaving,
 The establishment of a correct
diagnosis may be challenging

15. ABG INTERPRETATION
 Assessment of ABG
1. careful clinical evaluation
2. determine the primary acid–base disorder
3. evaluate the respiratory component
4. consider the metabolic component
5. consider the possibility of a mixed metabolic
acid–base disturbance
6. note the serum osmolal gap in any patient with
an unexplained high anion-gap acidosis
7. determine the cause of the identified processes

16. ABG INTERPRETATION
 Assessment of ABG
1. careful clinical evaluation
2. determine the primary acid–base disorder
3. evaluate the respiratory component
4. consider the metabolic component
5. consider the possibility of a mixed metabolic
acid–base disturbance
6. note the serum osmolal gap in any patient with
an unexplained high anion-gap acidosis
7. determine the cause of the identified processes

17. ABG INTERPRETATION
 Assessment of ABG
1. careful clinical evaluation
2. determine the primary acid–base disorder
3. evaluate the respiratory component
4. consider the metabolic component
5. consider the possibility of a mixed metabolic
acid–base disturbance
6. note the serum osmolal gap in any patient with
an unexplained high anion-gap acidosis
7. determine the cause of the identified processes

18. ABG INTERPRETATION
 signs and symptoms
 vital signs (which may indicate shock or sepsis),
 neurologic state
 signs of infection (e.g., fever),
 pulmonary status (respiratory rate, Kussmaul
respiration, cyanosis, clubbing of the fingers)
 gastrointestinal symptoms (vomiting and
diarrhea)
 pregnancy,
 diabetes,
 heart, lung, liver, and kidney disease,
 medications (e.g., laxatives, diuretics,
topiramate, or metformin)

19. ABG INTERPRETATION
 Assessment of ABG
1. careful clinical evaluation
2. determine the primary acid–base disorder
3. evaluate the respiratory component
4. consider the metabolic component
5. consider the possibility of a mixed metabolic
acid–base disturbance
6. note the serum osmolal gap in any patient with
an unexplained high anion-gap acidosis
7. determine the cause of the identified processes

20. ABG INTERPRETATION
Clinical Features of Respiratory Failure
Hypoxemic Hypercapnic
Cyanosis Flapping tremor of hands
Tachypnea Tachypnea
Tachycardia→arrhythmia→bradycardia Tachycardia
Peripheral vasoconstriction Peripheral vasodilation
warm hands/ headache
Restlessness→confusion→coma drowsiness→hallucination→coma
Sweating

21. ABG INTERPRETATION
 𝑷𝑷𝒂𝒂 𝑶𝑶𝟐𝟐 < 𝟓𝟓𝟓𝟓 𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎
 Memory defect, impaired judgement
 𝑷𝑷𝒂𝒂 𝑶𝑶𝟐𝟐 < 𝟒𝟒𝟒𝟒 𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎
 Tissue damage
 𝑷𝑷𝒂𝒂 𝑶𝑶𝟐𝟐 < 𝟑𝟑𝟑𝟑 𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎
 Unconsciousness
 𝑷𝑷𝒂𝒂 𝑶𝑶𝟐𝟐 < 𝟐𝟐𝟐𝟐 𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎
 Death

22. ABG INTERPRETATION
 Respiratory insufficiency:
 Low 𝑭𝑭𝒊𝒊 𝑶𝑶𝟐𝟐
 Hypoventilation
 𝑷𝑷𝒂𝒂 𝑪𝑪𝑪𝑪𝟐𝟐 = 𝑽𝑽𝑪𝑪𝑪𝑪𝟐𝟐/𝑽𝑽𝑽𝑽,
 𝑽𝑽/𝑸𝑸 mismatch
 Shunt
 (𝑷𝑷𝑨𝑨 𝑶𝑶𝟐𝟐 − 𝑷𝑷𝒂𝒂 𝑶𝑶𝟐𝟐)/𝟐𝟐𝟐𝟐
 Diffusion
 𝑫𝑫𝑫𝑫𝑫𝑫𝑫𝑫

23. ABG INTERPRETATION
 𝑷𝑷𝑨𝑨 𝑶𝑶𝟐𝟐 = 𝑭𝑭𝑭𝑭𝑭𝑭𝑭𝑭 × (𝑩𝑩𝑩𝑩– 𝑷𝑷𝑷𝑷𝑷𝑷𝑷𝑷)– (𝑷𝑷𝒂𝒂 𝑪𝑪𝑪𝑪𝟐𝟐/𝑹𝑹)
 𝑷𝑷𝑨𝑨 𝑶𝑶𝟐𝟐 = 𝑭𝑭𝑭𝑭𝑭𝑭𝑭𝑭 × 𝑩𝑩𝑩𝑩– 𝑷𝑷𝑷𝑷𝑷𝑷𝑷𝑷 – (𝟏𝟏. 𝟐𝟐𝟐𝟐 × 𝑷𝑷𝒂𝒂 𝑪𝑪𝑶𝑶𝟐𝟐)
 𝑩𝑩𝑩𝑩 = 𝟕𝟕𝟕𝟕𝟕𝟕𝟕𝟕𝟕𝟕𝟕𝟕𝟕𝟕, 𝑭𝑭𝑭𝑭𝑭𝑭𝑭𝑭 =? , 𝑷𝑷𝑷𝑷𝑷𝑷𝑷𝑷 = 𝟒𝟒𝟒𝟒𝟒𝟒𝟒𝟒𝟒𝟒𝟒𝟒 ,
𝑹𝑹 = 𝟎𝟎. 𝟖𝟖
 𝑰𝑰𝑰𝑰 𝑭𝑭𝑭𝑭𝑭𝑭𝑭𝑭 = 𝟐𝟐𝟐𝟐𝟐
 𝑷𝑷𝑨𝑨 𝑶𝑶𝟐𝟐 = 𝟏𝟏𝟏𝟏𝟏𝟏– (𝟏𝟏. 𝟐𝟐𝟐𝟐 × 𝑷𝑷𝒂𝒂 𝑪𝑪𝑪𝑪𝟐𝟐)

24. ABG INTERPRETATION
 In normal subjects:
 𝑷𝑷𝒂𝒂 𝑶𝑶𝟐𝟐 = 𝑭𝑭𝒊𝒊 𝑶𝑶𝟐𝟐 × 𝟓𝟓
 120 RULE:
 𝑷𝑷𝒂𝒂 𝑶𝑶𝟐𝟐 + 𝑷𝑷𝒂𝒂 𝑪𝑪𝑪𝑪𝟐𝟐=𝟏𝟏𝟏𝟏𝟏𝟏 ± 𝟏𝟏𝟏𝟏
 <120 venous admixture
 𝑷𝑷𝒂𝒂 𝑶𝑶𝟐𝟐 = 𝟏𝟏𝟏𝟏𝟏𝟏 − (𝟎𝟎. 𝟐𝟐𝟐𝟐 × 𝒂𝒂𝒂𝒂𝒂𝒂)
 𝑷𝑷𝑷𝑷𝑷𝑷𝑷𝑷/𝑭𝑭𝑭𝑭𝑭𝑭𝑭𝑭
 𝑵𝑵𝑵𝑵𝑵𝑵𝑵𝑵𝑵𝑵𝑵𝑵 𝟏𝟏𝟏𝟏𝟏𝟏/𝟎𝟎. 𝟐𝟐𝟐𝟐 = 𝟓𝟓𝟓𝟓𝟓𝟓
 𝟐𝟐𝟐𝟐𝟐𝟐 < 𝑷𝑷𝑷𝑷𝑷𝑷𝑷𝑷/𝑭𝑭𝑭𝑭𝑭𝑭𝑭𝑭 < 𝟑𝟑𝟑𝟑𝟑𝟑 𝑴𝑴𝑴𝑴𝑴𝑴𝑴𝑴 𝑨𝑨𝑨𝑨𝑨𝑨𝑨𝑨
 𝟏𝟏𝟏𝟏𝟏𝟏 < 𝑷𝑷𝑷𝑷𝑷𝑷𝑷𝑷/𝑭𝑭𝑭𝑭𝑭𝑭𝑭𝑭 < 𝟐𝟐𝟐𝟐𝟐𝟐 𝑴𝑴𝑴𝑴𝑴𝑴𝑴𝑴𝑴𝑴𝑴𝑴𝑴𝑴𝑴𝑴 𝑨𝑨𝑨𝑨𝑨𝑨𝑨𝑨
 𝑷𝑷𝑷𝑷𝑷𝑷𝑷𝑷/𝑭𝑭𝑭𝑭𝑭𝑭𝑭𝑭 < 𝟏𝟏𝟏𝟏𝟏𝟏 𝑺𝑺𝑺𝑺𝑺𝑺𝑺𝑺𝑺𝑺𝑺𝑺 𝑨𝑨𝑨𝑨𝑨𝑨𝑨𝑨
 (𝒐𝒐𝒐𝒐 𝑷𝑷𝑷𝑷𝑷𝑷𝑷𝑷 = 𝟓𝟓𝟓𝟓𝟓𝟓𝟓𝟓𝟓𝟓𝟓𝟓)

25. ABG INTERPRETATION
 (Alveolar-Arterial)O2=𝑷𝑷𝑨𝑨 𝑶𝑶𝟐𝟐 − 𝑷𝑷𝒂𝒂 𝑶𝑶𝟐𝟐:
 Young 𝟓𝟓 − 𝟏𝟏𝟏𝟏𝟏𝟏𝟏𝟏𝟏𝟏𝟏𝟏
 Old 𝟏𝟏𝟏𝟏 − 𝟐𝟐𝟐𝟐𝟐𝟐𝟐𝟐𝟐𝟐𝟐𝟐
 Increases with increase in 𝑭𝑭𝑭𝑭 𝑶𝑶𝟐𝟐
 For every decade, the alveolar–arterial
difference increases by 2 mm Hg
 𝑷𝑷𝑨𝑨 𝑶𝑶𝟐𝟐 − 𝑷𝑷𝒂𝒂 𝑶𝑶𝟐𝟐 = (𝑨𝑨𝑨𝑨𝑨𝑨/𝟒𝟒) + 𝟒𝟒
 𝑷𝑷𝑨𝑨 𝑶𝑶𝟐𝟐 − 𝑷𝑷𝒂𝒂 𝑶𝑶𝟐𝟐 = 𝟐𝟐. 𝟓𝟓 + (𝟎𝟎. 𝟐𝟐𝟐𝟐 × 𝒂𝒂𝒂𝒂𝒂𝒂 𝒊𝒊𝒊𝒊 𝒚𝒚𝒚𝒚𝒚𝒚𝒚𝒚𝒚𝒚)

26. ABG INTERPRETATION
𝑺𝑺𝒑𝒑 𝑶𝑶𝟐𝟐 𝒗𝒗𝒗𝒗 𝑺𝑺𝒂𝒂 𝑶𝑶𝟐𝟐
 𝑺𝑺𝒑𝒑 𝑶𝑶𝟐𝟐/𝑭𝑭𝑭𝑭𝑭𝑭𝑭𝑭 = 𝟐𝟐𝟐𝟐𝟐𝟐
 𝑷𝑷𝒂𝒂 𝑶𝑶𝟐𝟐/𝑭𝑭𝑭𝑭𝑭𝑭𝑭𝑭 = 𝟐𝟐𝟐𝟐𝟐𝟐
 𝑺𝑺𝒑𝒑 𝑶𝑶𝟐𝟐/𝑭𝑭𝑭𝑭𝑭𝑭𝑭𝑭 = 𝟑𝟑𝟑𝟑𝟑𝟑
 𝑷𝑷𝒂𝒂 𝑶𝑶𝟐𝟐/𝑭𝑭𝑭𝑭𝑭𝑭𝑭𝑭 = 𝟑𝟑𝟑𝟑𝟑𝟑

27. ABG INTERPRETATION
 Assessment of ABG
1. careful clinical evaluation
2. determine the primary acid–base disorder
3. consider the metabolic component
4. consider the possibility of a mixed metabolic
acid–base disturbance
5. note the serum osmolal gap in any patient with
an unexplained high anion-gap acidosis
6. evaluate the respiratory component
7. determine the cause of the identified processes

28. ABG INTERPRETATION
 The three major methods of
quantifying acid–base disorders:
 the physiological approach,
 the base-excess (BE) approach,
 the physicochemical approach (also
called the Stewart method)

29. ABG INTERPRETATION
 Based on the iso-hydric
principle,
 Acid: hydrogen-ion donor
 Base: hydrogen-ion acceptor
 Changes in [𝑯𝑯+
] alter virtually
all cellular function

30. ABG INTERPRETATION
 the normal plasma [𝑯𝑯+
]:
 very low 𝟒𝟒𝟒𝟒 𝒏𝒏𝒏𝒏𝒏𝒏𝒏𝒏/𝑳𝑳
 the pH
 −𝒍𝒍𝒍𝒍𝒍𝒍𝟏𝟏𝟏𝟏[𝑯𝑯+] = 𝒍𝒍𝒍𝒍𝒍𝒍𝟏𝟏𝟏𝟏
𝟏𝟏
[𝑯𝑯+]
 is generally used in clinical medicine to
indicate acid–base status.
 “acidemia”
 Plasma pH is abnormally low (acidic)
 “alkalemia”
 Plasma pH is abnormally high (alkaline)

31. ABG INTERPRETATION
 Acidemia vs Acidosis
 the hydrogen-ion concentration ↑
 Alkalemia vs Alkalosis
 the hydrogen-ion concentration ↓

32. ABG INTERPRETATION
the Henderson–Hasselbalch equation
𝒑𝒑𝒑𝒑 = 𝒑𝒑𝒑𝒑 + 𝒍𝒍𝒍𝒍𝒍𝒍𝟏𝟏𝟏𝟏(
𝑯𝑯𝑯𝑯𝑯𝑯𝑯𝑯−
𝟎𝟎. 𝟎𝟎𝟎𝟎 × 𝑷𝑷𝒂𝒂 𝑪𝑪𝑶𝑶𝟐𝟐
)
𝑯𝑯𝑯𝑯𝑯𝑯𝑯𝑯−
= proton acceptor = BASE (KIDNEY)
𝑪𝑪𝑪𝑪𝟐𝟐 = proton donor = ACID (LUNG)
𝒑𝒑𝒑𝒑 = 𝒑𝒑𝒑𝒑 + 𝒍𝒍𝒍𝒍𝒍𝒍𝟏𝟏𝟏𝟏([𝑩𝑩𝑩𝑩𝑩𝑩𝑩𝑩] / [𝑨𝑨𝑨𝑨𝑨𝑨𝑨𝑨])
𝒑𝒑𝒑𝒑 = 𝒑𝒑𝒑𝒑 + 𝒍𝒍𝒍𝒍𝒍𝒍𝟏𝟏𝟏𝟏([𝒌𝒌𝒌𝒌𝒌𝒌𝒌𝒌𝒌𝒌𝒌𝒌] / [𝒍𝒍𝒍𝒍𝒍𝒍𝒍𝒍])

33. ABG INTERPRETATION
 Assessment of ABG
1. careful clinical evaluation
2. determine the primary acid–base disorder
3. evaluate the respiratory component
4. consider the metabolic component
5. consider the possibility of a mixed metabolic
acid–base disturbance
6. note the serum osmolal gap in any patient with
an unexplained high anion-gap acidosis
7. determine the cause of the identified processes

34. ABG INTERPRETATION
 pH = pK + log10 ([kidney] / [lung])
 ACIDOSIS:
 Respiratory
 Metabolic
 ALKALOSIS:
 Respiratory
 Metabolic

35. ABG INTERPRETATION
 Metabolic acidosis
 𝒑𝒑𝒑𝒑 < 𝟕𝟕. 𝟑𝟑𝟑𝟑 and [𝑯𝑯𝑯𝑯𝑯𝑯𝑯𝑯−
] < 𝟐𝟐𝟐𝟐 𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎/𝒍𝒍𝒍𝒍𝒍𝒍𝒍𝒍𝒍𝒍
𝑩𝑩𝑩𝑩 < −𝟐𝟐 𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎/𝒍𝒍𝒍𝒍𝒍𝒍𝒍𝒍𝒍𝒍
 Secondary (respiratory) response:
 𝑷𝑷𝒂𝒂 𝑪𝑪𝑶𝑶𝟐𝟐 = 𝟏𝟏. 𝟓𝟓 × [𝑯𝑯𝑯𝑯𝑯𝑯𝑯𝑯−] + 𝟖𝟖 ± 𝟐𝟐 𝒎𝒎𝒎𝒎 𝑯𝑯𝑯𝑯
or
 𝑷𝑷𝒂𝒂 𝑪𝑪𝑶𝑶𝟐𝟐 = [𝑯𝑯𝑯𝑯𝑯𝑯𝑯𝑯−] + 𝟏𝟏𝟏𝟏 𝒎𝒎𝒎𝒎 𝑯𝑯𝑯𝑯
 Complete secondary adaptive response within 12–24 hr

36. ABG INTERPRETATION
 Metabolic alkalosis
 𝒑𝒑𝒑𝒑 > 𝟕𝟕. 𝟒𝟒𝟒𝟒 and [𝑯𝑯𝑯𝑯𝑯𝑯𝑯𝑯−] > 𝟐𝟐𝟐𝟐 𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎/𝒍𝒍𝒍𝒍𝒍𝒍𝒍𝒍𝒍𝒍
𝑩𝑩𝑩𝑩 > +𝟐𝟐 𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎/𝒍𝒍𝒍𝒍𝒍𝒍𝒍𝒍𝒍𝒍
 Secondary (respiratory) response:
 𝑷𝑷𝒂𝒂 𝑪𝑪𝑶𝑶𝟐𝟐 = 𝟎𝟎. 𝟕𝟕 × ([𝑯𝑯𝑯𝑯𝑯𝑯𝑯𝑯−] − 𝟐𝟐𝟐𝟐) + 𝟒𝟒𝟒𝟒 ± 𝟐𝟐 𝒎𝒎𝒎𝒎 𝑯𝑯𝑯𝑯
or
 𝑷𝑷𝒂𝒂 𝑪𝑪𝑶𝑶𝟐𝟐 = [𝑯𝑯𝑯𝑯𝑯𝑯𝑯𝑯−
] + 𝟏𝟏𝟏𝟏 𝒎𝒎𝒎𝒎 𝑯𝑯𝑯𝑯
or
 𝑷𝑷𝒂𝒂 𝑪𝑪𝑶𝑶𝟐𝟐 = 𝟎𝟎. 𝟕𝟕 × [𝑯𝑯𝑯𝑯𝑯𝑯𝑯𝑯−
] + 𝟐𝟐𝟐𝟐 𝒎𝒎𝒎𝒎 𝑯𝑯𝑯𝑯
 Complete secondary adaptive response within 24–36 hr

37. ABG INTERPRETATION
 Respiratory acidosis
 𝒑𝒑𝒑𝒑 < 𝟕𝟕. 𝟑𝟑𝟑𝟑 𝒂𝒂𝒂𝒂𝒂𝒂 𝑷𝑷𝑷𝑷𝑷𝑷𝑷𝑷𝑷𝑷 > 𝟒𝟒𝟒𝟒 𝒎𝒎𝒎𝒎 𝑯𝑯𝑯𝑯
 Secondary (metabolic) response
 Acute:
 ∆𝑷𝑷𝒂𝒂 𝑪𝑪𝑶𝑶𝟐𝟐 = ↑ 𝟏𝟏𝟏𝟏 𝒎𝒎𝒎𝒎 𝑯𝑯𝑯𝑯 𝒂𝒂𝒂𝒂𝒂𝒂𝒂𝒂𝒂𝒂 𝟒𝟒𝟒𝟒 𝒎𝒎𝒎𝒎 𝑯𝑯𝑯𝑯
→ ∆ 𝑯𝑯𝑯𝑯𝑯𝑯𝑯𝑯−
= ↑ 𝟏𝟏
𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎
𝑳𝑳
 Chronic:
 ∆𝑷𝑷𝒂𝒂 𝑪𝑪𝑶𝑶𝟐𝟐 = ↑ 𝟏𝟏𝟏𝟏 𝒎𝒎𝒎𝒎 𝑯𝑯𝑯𝑯 𝒂𝒂𝒂𝒂𝒂𝒂𝒂𝒂𝒂𝒂 𝟒𝟒𝟒𝟒 𝒎𝒎𝒎𝒎 𝑯𝑯𝑯𝑯
→ ∆ 𝑯𝑯𝑯𝑯𝑯𝑯𝑯𝑯−
= ↑ 𝟐𝟐 − 𝟒𝟒
𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎
𝑳𝑳
 Complete secondary adaptive response within 2–5 days

38. ABG INTERPRETATION
 Respiratory alkalosis
 𝒑𝒑𝒑𝒑 > 𝟕𝟕. 𝟒𝟒𝟒𝟒 𝒂𝒂𝒂𝒂𝒂𝒂 𝑷𝑷𝑷𝑷𝑷𝑷𝑷𝑷𝑷𝑷 < 𝟑𝟑𝟑𝟑 𝒎𝒎𝒎𝒎 𝑯𝑯𝑯𝑯
 Secondary (metabolic) response
 Acute:
 ∆𝑷𝑷𝒂𝒂 𝑪𝑪𝑶𝑶𝟐𝟐 = ↓ 𝟏𝟏𝟏𝟏 𝒎𝒎𝒎𝒎 𝑯𝑯𝑯𝑯 𝒃𝒃𝒃𝒃𝒃𝒃𝒃𝒃𝒃𝒃 𝟒𝟒𝟒𝟒 𝒎𝒎𝒎𝒎 𝑯𝑯𝑯𝑯
→ ∆ 𝑯𝑯𝑯𝑯𝑯𝑯𝑯𝑯−
= ↓ 𝟐𝟐
𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎
𝑳𝑳
 Chronic:
 ∆𝑷𝑷𝒂𝒂 𝑪𝑪𝑶𝑶𝟐𝟐 = ↓ 𝟏𝟏𝟏𝟏 𝒎𝒎𝒎𝒎 𝑯𝑯𝑯𝑯 𝒃𝒃𝒃𝒃𝒃𝒃𝒃𝒃𝒃𝒃 𝟒𝟒𝟒𝟒 𝒎𝒎𝒎𝒎 𝑯𝑯𝑯𝑯
→ ∆ 𝑯𝑯𝑯𝑯𝑯𝑯𝑯𝑯−
= ↓ 𝟒𝟒 − 𝟓𝟓
𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎
𝑳𝑳
 Complete secondary adaptive response within 2–5 days

39. ABG INTERPRETATION
 Met Acidosis:
 𝒍𝒍𝒍𝒍𝒍𝒍 𝒑𝒑𝒑𝒑 𝒂𝒂𝒂𝒂𝒂𝒂 𝒍𝒍𝒍𝒍𝒍𝒍 𝒃𝒃𝒃𝒃𝒃𝒃𝒃𝒃𝒃𝒃𝒃𝒃
 Met Alkalosis:
 𝒉𝒉𝒉𝒉𝒉𝒉𝒉𝒉 𝒑𝒑𝒑𝒑 𝒂𝒂𝒂𝒂𝒂𝒂 𝒉𝒉𝒉𝒉𝒉𝒉𝒉𝒉 𝒃𝒃𝒃𝒃𝒃𝒃𝒃𝒃𝒃𝒃𝒃𝒃
 Resp Acidosis:
 𝒍𝒍𝒍𝒍𝒍𝒍 𝒑𝒑𝒑𝒑 𝒂𝒂𝒂𝒂𝒂𝒂 𝒉𝒉𝒉𝒉𝒉𝒉𝒉𝒉 𝑷𝑷𝒂𝒂 𝑪𝑪𝑶𝑶𝟐𝟐
 Resp Alkalosis:
 𝒉𝒉𝒉𝒉𝒉𝒉𝒉𝒉 𝒑𝒑𝒑𝒑 𝒂𝒂𝒂𝒂𝒂𝒂 𝒍𝒍𝒍𝒍𝒍𝒍 𝑷𝑷𝒂𝒂 𝑪𝑪𝑶𝑶𝟐𝟐

40. ABG INTERPRETATION
 Assessment of ABG
1. careful clinical evaluation
2. determine the primary acid–base disorder
3. evaluate the respiratory component
4. consider the metabolic component
5. consider the possibility of a mixed metabolic
acid–base disturbance
6. note the serum osmolal gap in any patient with
an unexplained high anion-gap acidosis
7. determine the cause of the identified processes

41. ABG INTERPRETATION
 Calculation of the anion gap:
 [𝑵𝑵𝑵𝑵+
] + [𝑲𝑲+
] + [𝑪𝑪𝑪𝑪𝟐𝟐+
] + [𝑴𝑴𝑴𝑴𝟐𝟐+
] + + [𝑯𝑯+
]
+ 𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖 𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄𝒄 = [𝑪𝑪𝑪𝑪−
] + [𝑯𝑯𝑪𝑪𝑪𝑪𝟑𝟑
−
]
+ [𝑪𝑪𝑪𝑪𝟑𝟑
𝟐𝟐−
] + [𝑶𝑶𝑶𝑶−
] + 𝒂𝒂𝒂𝒂𝒂𝒂𝒂𝒂𝒂𝒂𝒂𝒂𝒂𝒂
+ 𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑𝒑 + 𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔𝒔 + 𝒍𝒍𝒍𝒍𝒍𝒍𝒍𝒍𝒍𝒍𝒍𝒍𝒍𝒍
+ 𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖𝒖 𝒂𝒂𝒂𝒂𝒂𝒂𝒂𝒂𝒂𝒂𝒂𝒂
 𝑨𝑨𝑨𝑨𝑨𝑨𝑨𝑨𝑨𝑨 𝑮𝑮𝑮𝑮𝑮𝑮 = [𝑵𝑵𝑵𝑵+
] − ([𝑪𝑪𝑪𝑪−
] + [𝑯𝑯𝑪𝑪𝑪𝑪𝟑𝟑
−
])
 = 𝑼𝑼𝑼𝑼 − 𝑼𝑼𝑼𝑼
 = 𝟏𝟏𝟏𝟏 − 𝟏𝟏𝟏𝟏𝟏𝟏𝟏𝟏𝟏𝟏/𝑳𝑳

42. ABG INTERPRETATION

43. ABG INTERPRETATION
 High anion-gap metabolic acidosis
 GOLD MARRK
 Glycols [ethylene and propylene],
 5-oxoproline [pyroglutamic acid],
 l-lactate,
 d-lactate,
 methanol,
 aspirin,
 renal failure,
 rhabdomyolysis,
 ketoacidosis

44. ABG INTERPRETATION
 Normal Anion Gap Acidosis:
 GI or Urinary HCO3- loss
 Urinary Anion GAP:
 ( 𝑵𝑵𝑵𝑵+
+ 𝑲𝑲+
)– [𝑪𝑪𝑪𝑪−
]
 neGUTive GI (diarrhea), PRTA
 Positive in RF, DRTA, Hypoaldosteronism

45. ABG INTERPRETATION
 Normal Anion Gap Acidosis:
 DURHAM:
 Diarrhea
 Uremia
 RTA
 Hyperalimentation
 Acetazolamide
 Miscellaneous

46. ABG INTERPRETATION
 Metabolic Alkalosis:
 Gastric fluid loss
 Diuretic
 Urinary Chloride:
 < 𝟐𝟐𝟐𝟐𝟐𝟐𝟐𝟐𝟐𝟐𝟐𝟐/𝑳𝑳
 > 𝟒𝟒𝟒𝟒𝟒𝟒𝟒𝟒𝟒𝟒𝟒𝟒/𝑳𝑳 (𝒉𝒉𝒉𝒉𝒉𝒉𝒉𝒉 𝑲𝑲, 𝑯𝑯𝑯𝑯𝑯𝑯𝑯𝑯𝑯𝑯 𝑨𝑨𝑨𝑨𝑨𝑨𝑨𝑨𝑨𝑨)

47. ABG INTERPRETATION
 Physiotherapy is safe and efficient in critically
ill patients
 During mechanical ventilation chest
physiotherapy with positioning is very useful
in pulmonary diseases
 Early and safe mobilization is important in
intubated and critically ill patients
 The volume therapy/NIPPV with positioning
and manual therapy is efficient in the weaning
process
 Hemodynamic & ABG monitoring is necessary

48. ABG INTERPRETATION
 Case1: 57 year old lady, day 3 post-
cholecystectomy, complaining of
breathlessness.
 Her ABG:
 𝒑𝒑𝒑𝒑: 𝟕𝟕. 𝟒𝟒𝟒𝟒 (𝟕𝟕. 𝟑𝟑𝟑𝟑 − 𝟕𝟕. 𝟒𝟒𝟒𝟒)
 𝑷𝑷𝒂𝒂 𝑶𝑶𝟐𝟐: 𝟓𝟓𝟓𝟓𝟓𝟓𝟓𝟓𝟓𝟓𝟓𝟓 (𝟖𝟖𝟖𝟖 − 𝟏𝟏𝟏𝟏𝟏𝟏)
 𝑷𝑷𝒂𝒂 𝑪𝑪𝑶𝑶𝟐𝟐: 𝟑𝟑𝟑𝟑𝟑𝟑𝟑𝟑𝟑𝟑𝟑𝟑 (𝟑𝟑𝟑𝟑 − 𝟒𝟒𝟒𝟒)
 𝑯𝑯𝑯𝑯𝑯𝑯𝑯𝑯: 𝟐𝟐𝟐𝟐𝟐𝟐𝟐𝟐𝟐𝟐𝟐𝟐/𝒍𝒍 (𝟐𝟐𝟐𝟐 − 𝟐𝟐𝟐𝟐)
 𝑩𝑩𝑩𝑩: −𝟏𝟏𝟏𝟏𝟏𝟏𝟏𝟏𝟏𝟏/𝒍𝒍 (−𝟐𝟐 𝒕𝒕𝒕𝒕 + 𝟐𝟐)
 Other values within normal range

49. ABG INTERPRETATION
 Case 1:Type 1 respiratory
failure.The PO2 is low in
accompanying with a low
CO2.
 The accompanying alkalosis is
a response, due to the patient
blowing off CO2 due to her
likely high respiratory rate.

50. ABG INTERPRETATION
 Case 2: A 79 year old man is
being assessed. His ABG is as
follows:
 𝒑𝒑𝒑𝒑: 𝟕𝟕. 𝟑𝟑𝟑𝟑 (𝟕𝟕. 𝟑𝟑𝟑𝟑 − 𝟕𝟕. 𝟒𝟒𝟒𝟒)
 𝑷𝑷𝒂𝒂 𝑶𝑶𝟐𝟐: 𝟔𝟔𝟔𝟔𝟔𝟔𝟔𝟔𝟔𝟔𝟔𝟔 (𝟏𝟏𝟏𝟏– 𝟏𝟏𝟏𝟏)
 𝑷𝑷𝒂𝒂 𝑪𝑪𝑶𝑶𝟐𝟐: 𝟔𝟔𝟔𝟔𝟔𝟔𝟔𝟔𝟔𝟔𝟔𝟔 (𝟑𝟑𝟑𝟑 − 𝟒𝟒𝟒𝟒)
 𝑯𝑯𝑯𝑯𝑯𝑯𝑯𝑯: 𝟑𝟑𝟑𝟑𝟑𝟑𝟑𝟑𝟑𝟑𝟑𝟑/𝒍𝒍 (𝟐𝟐𝟐𝟐 − 𝟐𝟐𝟐𝟐)
 𝑩𝑩𝑩𝑩: +𝟓𝟓 𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎/𝒍𝒍(−𝟐𝟐 𝒕𝒕𝒕𝒕 + 𝟐𝟐)
 Other values within normal range

51. ABG INTERPRETATION
 Case 2:Type 2 respiratory failure.The
PO2 ↓ with CO2 ↑.
 pH: normal: Compensated respiratory
acidosis.
 No acute pathology.
 a compensation for a chronic
respiratory acidosis secondary to
chronic pulmonary disease.
 Note this is an acidosis, not an
acidemia (pH normal, but only due to
compensatory mechanisms: the high
bicarbonate).

52. ABG INTERPRETATION
 Case 3: A 67 year old man with a
Hx COPD, worsening shortness
of breath and increased Sputum
production.
 𝒑𝒑𝒑𝒑: 𝟕𝟕. 𝟐𝟐𝟐𝟐 (𝟕𝟕. 𝟑𝟑𝟑𝟑 − 𝟕𝟕. 𝟒𝟒𝟒𝟒)
 𝑷𝑷𝒂𝒂 𝑶𝑶𝟐𝟐: 𝟓𝟓𝟓𝟓 𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎 (𝟖𝟖𝟖𝟖 − 𝟏𝟏𝟏𝟏𝟏𝟏)
 𝑷𝑷𝒂𝒂 𝑪𝑪𝑶𝑶𝟐𝟐: 𝟔𝟔𝟔𝟔 𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎 (𝟑𝟑𝟑𝟑 − 𝟒𝟒𝟒𝟒)
 𝑯𝑯𝑯𝑯𝑯𝑯𝑯𝑯: 𝟐𝟐𝟐𝟐 𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎/𝒍𝒍(𝟐𝟐𝟐𝟐 − 𝟐𝟐𝟐𝟐)
 𝑩𝑩𝑩𝑩: +𝟒𝟒 𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎/𝒍𝒍(−𝟐𝟐 𝒕𝒕𝒕𝒕 + 𝟐𝟐)
 Other values within normal range

53. ABG INTERPRETATION
 Case 3:Type 2 respiratory failure.
 HCO3 ↑despite the abnormal pH.
 likely to represent an acute on
chronic respiratory acidosis.
 This would indicate that the
patient normally retains CO2 and
has a chronically raised HCO3.
 The drop in pH represents the
normal mechanisms of
decompensation over old
compensation.

54. ABG INTERPRETATION
 Case 4: A 67 year-old man , Hx
peptic ulcer disease, and
persistent vomiting.
 𝒑𝒑𝒑𝒑: 𝟕𝟕. 𝟓𝟓𝟓𝟓 (𝟕𝟕. 𝟑𝟑𝟑𝟑 − 𝟕𝟕. 𝟒𝟒𝟒𝟒)
 𝑷𝑷𝒂𝒂 𝑶𝑶𝟐𝟐: 𝟖𝟖𝟖𝟖 𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎(𝟖𝟖𝟖𝟖 − 𝟏𝟏𝟏𝟏𝟏𝟏)
 𝑷𝑷𝒂𝒂 𝑪𝑪𝑶𝑶𝟐𝟐: 𝟑𝟑𝟑𝟑 𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎(𝟑𝟑𝟑𝟑 − 𝟒𝟒𝟒𝟒)
 𝑯𝑯𝑯𝑯𝑯𝑯𝑯𝑯: 𝟑𝟑𝟑𝟑 𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎/𝒍𝒍 (𝟐𝟐𝟐𝟐 − 𝟐𝟐𝟐𝟐)
 𝑩𝑩𝑩𝑩: +𝟔𝟔 𝒎𝒎𝒎𝒎𝒎𝒎𝒎𝒎/𝒍𝒍 (−𝟐𝟐 𝒕𝒕𝒕𝒕 + 𝟐𝟐)
 Other values within normal
range

55. ABG INTERPRETATION
 Case 4:This is metabolic alkalemia
 Dx:
 Persistent vomiting
 E.g. gastric outlet obstruction
 Hyperaldosteronaemia
 Diuretic use
 Milk alkali syndrome
 Massive transfusion

56. ABG INTERPRETATION
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