Arterial Blood Gas

Jaime C. Tan,MD
Division of Pulmonary and Critical Care
Medicine
Philippine Heart center
 Indications of ABG
 Determine acid-base or
oxygenation problem
 May indicate onset or culmination

of cardiopulmonary crises
 May serve as a gauge to the

appropriateness or effectiveness of
therapy
 Normal ABG Values

pH 7.35 – 7.45
PaCO2 35 – 45 mmHg
[BE] 0  2 meq/L
PaO2 80 – 100 mmHg
[HCO3] 24  2 meq/L
SaO2 97 – 98%
Steps for the interpretation of acid base
disturbance
 Is the px acidemic or alkalemic?
 Is the disturbance respiratory or

metabolic?
 If the disturbance is respiratory, is it

acute or chronic?
 If the disturbance is metabolic, is

the anion gap normal or abnormal?

 If the disturbance is metabolic, is the
respiratory system compensating?
 Severity of Generalized Acid-
Base Disturbances
pH Degree of Impairment
< 7.20 Severe acidemia
7.20 – 7.29 Moderate acidemia
7.30 – 7.34 Mild acidemia
7.35 – 7.45 Normal pH
7.46 – 7.50 Mild alkalemia
7.51 – 7.55 Moderate alkalemia
> 7.55 Severe alkalemia
 Classification of PaO2
in the Adult
Classification PaO2 (mmHg)

Hyperoxemia >100

Normoxemia 80 – 100

Mild hypoxemia 60 – 79

Moderate hypoxemia 45 – 59

Severe hypoxemia < 45

 Room Air (Fio2=.21)
 Px < 60 y.o. = Po2 =80-100mhg
 Px >60 y.o. = subtract 1 from 80 for

every year above 60 years of age

example: 70 y.o.
Ideal PaO2= 80
- 10
------
70 mmhg
 Supplemental O2
 Fio2= Lpm x 4 + 20
 P/F ratio: PaO2/ FiO2
 NV: <60 y.o.= 400-500
 NV:>60 y.o.= multiply every year above 60 by
5 then subtract the total from 400
ex: 70y.o.
= 10x 5= 50
= 400-50
= 350
 Steps in analyzing the oxygenation
status
 Is the px hypoxemic or non hypoxemic ?
PaO2, Fio2, P/F ratio

Ex: 75 yo, 2 lpm

actual P/F= 296
expected P/F= 325
Therefore the px is HYPOXEMIC
 If the px is hypoxemic, is it corrected,
uncorrected or overcorrected?
Compute for pO2 expected for age:
ex: 75 y.o., PaO2: 80
expected Po2 for age:80-15=65
px has CORRECTED HYPOXEMIA
 If the px is non hypoxemic , is he receiving
adequate oxygenation or more than adequate
oxygenation?
Ex: 75y.o., actual Po2:109, Fio2: 0.28, P/F
ratio:389 (expected:325)
px is NON HYPOXEMIC
expected Po2 for age:65, actual Po2: 109
Receiving MORE THAN ADEQUATE
OXYGENATION
 Acid-Base Classification
Acid-base disturbance pH PaCO2 HCO3

Respiratory acidosis   N0 or 

Respiratory alkalosis   N0 or 

Metabolic acidosis  N0 or  

Metabolic alkalosis  N0 or  
Cases
 Case
V.M., 59 year old male
 Moderate COPD; NIDDM
 2-week cough with yellow sputum

 Intermittent low-grade fever

 Cefuroxime, Paracetamol,
x 3 days
Fenoterol+Ipratropium Br
 Sought consult at ER due to dyspnea

and pleuritic chest pain

 Case
 At ER, he was agitated with the ff v/s:
BP 130/90mmHg HR 110/min
RR 28/min T 380C
 Chest/Lungs: increased breath

sounds and tactile fremitus at the

right lower lung field, crackles on
both lower lung fields
 Case
 Chest x-ray: lobar pneumonia at the
right lower lobe, hazy densities at the
left base and blunting of the right
costophrenic angle
 Case
 ABG taken at room air
pH 7.50
PaCO2 31 mmHg
PaO2 60 mmHg
HCO3 20 meq/L
BE 1.6 meq/L
SaO2 90%
What is the acid-base problem?
A. Respiratory alkalosis
B. Respiratory acidosis
C. Metabolic
A. alkalosisalkalosis
Respiratory
D. Metabolic acidosis
 Respiratory Alkalosis
 Hallmark

 pH,  PaCO2
 Compensation

 Cellular buffering
 Renal
response: retention of
endogenous acids, excretion of
HCO3
 Respiratory Alkalosis
 Formula for compensation

HCO3  by 2 - 4 meq/L
 Respiratory Alkalosis
Primary central disorders Hypoxia
 Hyperventilation
Septicemia, hypotension
syndrome, anxiety
Hepatic failure
 Cerebrovascular disease

 Meningitis, encephalitis
Drugs
 Salicylates
Pulmonary disease
 Nicotine
 Interstitial fibrosis

 Pneumonia  Xanthines

 Pulmonary embolism  Progestational hormones

 Pulmonary edema (some High altitude

patients) Mechanical ventilators
 Respiratory Alkalosis
 Treatment
 Treat the primary cause
 Control the patient’s ventilation
 Paralyze the patient
 CMV

 Carbonic anhydrase inhibitor

(acetazolamide)
 To decrease HCO3 of limited value

* Most frequently, requires no specific therapy

 Case
 Given O2 at 4L/min via nasal cannula
 SaO2 98%
 Given Ceftazidime, Amikacin
WBC 30 x 106/uL
Segmenters 98%; (+) toxic granules
Potassium 4 mmol/L
Sodium 135 mmol/L
Creatinine 0.12 mmol/L
 Case
 Eight hours later  drowsy with
labored breathing and cyanosis
 ABG at 10L/min O2
pH 7.23
PaCO2 86 mmHg
PaO2 69 mmHg
HCO3 25 meq/L
BE - 4.8 meq/L
SaO2 91%
 Case
 Repeat Chest X-Ray: progression of
hazy densities on the left lower lung
field, with no significant interval
change in the previously noted right
lower lobe pneumonia.
 Patient admitted to ICU
What is the acid-base problem?
A. Respiratory alkalosis
B. Respiratory acidosis
C. Metabolic
B. alkalosisacidosis
Respiratory
D. Metabolic acidosis
 Respiratory Acidosis
 Hallmark

 pH,  PaCO2
 Compensation

 Cellular buffering:  HCO3

 Renal adaptation:  H+ secretion,
 Cl- reabsorption,  net acid
excretion
 Respiratory Acidosis
 Formula for compensation

HCO3  by 3 - 4 meq/L
 Respiratory Acidosis
 COPD  Neuromuscular disease
 O2 excess in COPD  Poliomyelitis
 ALL
 Drugs
 G-B syndrome
 Barbiturates
 Electrolyte deficiencies
 Anesthetics
(K+, PO4-)
 Narcotics  Myasthenia gravis
 Sedatives
 Excessive CO2
 Extreme ventilation- production
perfusion mismatch  TPN
 Exhaustion  Sepsis
 Inadequate MV  Severe burns
 Neurologic disorders  NaHCO3 administration
 Respiratory Acidosis
 Treatment:

 Correct precipitating cause

 Restore alveolar ventilation

 Correct CO2 retention

 Intubationand assisted ventilation

 O2 administration
 Case
 Third ICU day
 blood C/S: Klebsiella pneumoniae
 Sensitive:
piperacillin/tazobactam,
meropenem, cefepime
 Resistant: ceftazidime, amikacin
 Decreasing urine output at 10ml/hr
 Impression: acute renal failure
 Referred to nephrologist
 Case

 Laboratories

sodium 145 mmol/L

potassium 5 mmol/L
chloride 106 mmol/L
creatinine 0.48 mmol/L
CBG 300 mg/dL
 Case
 ABG at 40% FiO2, BUR 20/min
400ml VT, PEEP 5cmH2O
pH 7.20
PaCO2 25 mmHg
PaO2 114 mmHg
HCO3 11 meq/L
BE - 15.9 meq/L
SaO2 98.4%
What is the acid-base problem?
A. Respiratory alkalosis
B. Respiratory acidosis
C. Metabolic alkalosis
D. Metabolic acidosis
D. Metabolic acidosis
Metabolic Acidosis
 Metabolic Acidosis
Hallmark:
  pH

 HCO3

 basedeficit
 accumulation of fixed acids
 Metabolic Acidosis
Abnormalities:
 Overproduction of acids

 Loss of buffer stores

 Underexcretion of acids
 Metabolic Acidosis
Compensation
  pCO2 (hyperventilation)

 Pathway:
 HCO3  pCO2 ratio  H+ conc
HCO3
Acidification of ECF  ECF  pH

Stimulation of brainstem  RR  pCO2

Normalization of pH
 Metabolic Acidosis
Compensation
 Ionic shift

 K+moves extracellularly for H+

 HCO3 generation, H+ excretion
 Metabolic Acidosis
Effects
 Stimulate epinephrine release

 Leukocytosis

 Hyperkalemia

 Hypercalcemia / hypercalciuria

 Myocardial failure
 Anion Gap
 Numerical
difference between Na+
and HCO3, Cl-
 Helpfultool in suggesting the
presence and clarifying the
differential diagnosis of metabolic
acidosis
Anion Gap = [Na+] – [HCO3 + Cl-]
N0 value = 12  2 meq/L
 Normal vs. Elevated Anion Gap
Normal Anion Gap
 Reduced HCO3 is counterbalanced by a

measurable anion
 GI disorders (diarrhea, pancreatic fistulas)
 Uterosigmoidoscopy, ileostomy

 Ingestion of acids, parenteral

hyperalimentation
 Carbonic anhydrase inhibitors

 Renal acidification defects

 Normal vs. Elevated Anion Gap

Elevated Anion Gap

 Reduced HCO3 is replaced by an

unmeasurable organic anion

 Ketoacidosis (starvation, alcohol-induced)
 Lactic acidosis

 Chronic renal failure

 Methyl alcohol / ethyl alcohol ingestion

 Paraldehyde ingestion

 Salicylate overdose
 Metabolic Acidosis
 Compensation

Expected pCO2 = HCO3 x 1.5 + 8.4

Limit = 10 mmHg
 Metabolic Acidosis
Management
 Sustain normality of blood acid base

parameters
 Maintain serum HCO3 = 10 to 15 meq/L
 HCO3 administration for pH < 7.2
 Treat the underlying cause
 NaHCO3 Deficit Computation

HCO3 = (desired – actual HCO3) x 0.4 x wt (kg)

HCO3 = BE x 0.3 x wt (kg)

2
 Case
 Urine output improved after fluid
challenge
 Few hours later  tachypneic

 PEEP increased to 8 cmH2O

pH 7.36
PaCO2 34 mmHg
PaO2 89 mmHg
HCO3 18 meq/L
BE - 6.1 meq/L
SaO2 96.6%
 Case
 Furosemide drip started at 10mg/hr
 Laboratories:

sodium 140 mmol/L

potassium 2 mmol/L
chloride 100 mmol/L
creatinine 0.34 mmol/L
albumin 26 g/dL
 Case
 Repeat ABG at 40% FiO2, VT 400ml,
BUR 20/min, PEEP 8cmH2O
pH 7.53
PaCO2 47 mmHg
PaO2 109 mmHg
HCO3 36 meq/L
BE 11.3 meq/L
SaO2 98.5%
What is the acid-base problem?
A. Respiratory alkalosis
B. Respiratory acidosis
C. Metabolic alkalosis
C. Metabolic alkalosis
D. Metabolic acidosis
 Metabolic Alkalosis
 Hallmark

 pH,  HCO3

 Compensation

 PaCO2 (hypoventilation)
 Metabolic Alkalosis
 Pathway

 HCO3 PaCO2  H+ conc

ratio
HCO3

Alkalinization of ECF  PaCO2 with mild hypoxemia

Normalization of pH
 Metabolic Alkalosis
 Compensation

Expected PaCO2= ( O.8 x HCO3 ) + 16  4

 Every 1 mEq increase in HCO3 will

increase PaCO2 by 0.5-1 mmHg
 Causes of Metabolic Alkalosis
Hypokalemia*
Ingestion of large amounts of alkali or licorice
Gastric fluid loss: Vomiting, NG suctioning*
Hyperaldosteronism 20 to nonadrenal factors
Bartter’s syndrome
Inadequate renal perfusion
diuretics (inhibiting NaCl reabsorption)*
Bicarbonate administration
Sodium bicarbonate overcorrection
Blood transfusion
Adrenocortical hypersecretion (e.g tumor)
Steroids*
Eucapnic ventilation posthypercapnia

* Common in the ICU

 Treatment of
Metabolic Alkalosis
 Replace fluids (with Normal Saline)
 Replace electrolyte deficit

 K supplementation (K > 4.5 mEq/L)

 Ammonium chloride

 Hydrochloric acid

 Acetazolamide (carbonic anhydrase

inhibitor) -promotes renal excretion
of HCO3-
 Sample problem:
 68 y.o., male, w/ increasing SOB,
admitted at ER, initial ABG: (32% fio2)
 Ph: 7.25, Pco2: 75, Po2= 95,HCO3: 32,

O2 sat: 94%
 Role of Nurses
 Evaluation of symptoms
 When to refer to MD
 Administration of medications
 Awareness of potential
complications of medications
 Evaluation of Symptoms
 Respiratory acidosis
 Alteration of state of consciousness
 Confusion

 Stupor

 Obtundation

 Coma
 Evaluation of Symptoms
 Respiratory alkalosis
 Cerebral vasoconstriction
 Nausea, vomiting, lightheadedness

 Carpopedal spasm
 Circumoral, digital paresthesias
 Evaluation of Symptoms
 Metabolic alkalosis
 Increase neuromuscular activity
 Chvostek, Trousseau sign
 Twitching, tetany

 Arrhythmias
 Evaluation of Symptoms
 Metabolic acidosis
 Kussmaul’s respiration
 Hyperpnea, tachypnea

 Hypotension
 Arrhythmias
 Administration of Medications
 Sodium Bicarbonate
 Given for correction of metabolic
acidosis
 Bicarbonate deficit
HCO3 = BE x 0.3 x wt (kg)
2

HCO3 = (desired – actual HCO3) x 0.4 x wt (kg)

 Potential Complications of Medications

 Local site complication

 Patent IV site

 Bicarbonate overcorrection
 Hypokalemia
 Fluid overload or hypernatremia
Thank You for
Listening